Traxcess-14 Microguidewire-Assisted Electrocoagulation as a Therapeutic Option for Basilar Artery Pseudoaneurysm: A Case Report

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Neurointervention. 2026;21(1):53-57

Publication date (electronic) : 2026 January 15

doi : https://doi.org/10.5469/neuroint.2025.01109

Zifeng Dai, MD^,*, Junjun Zhang, MSc^,*, Jianfei Zhang, MSc, Fanyong Gong, MSc, Shengjun Zhou, MD

Department of Neurosurgery, First Affiliated Hospital of Ningbo University, Ningbo, China

Correspondence to: Shengjun Zhou, MD Department of Neurosurgery, First Affiliated Hospital of Ningbo University, 59 Liuting Street, Haishu District, Ningbo City, Zhejiang Province 30015, China E-mail: fyyzhoushengjun@nbu.edu.cn

*These authors contributed equally to the manuscript as first author.

Received 2025 November 27; Revised 2025 December 31; Accepted 2026 January 5.

Abstract

INTRODUCTION

Spontaneous subarachnoid hemorrhage (SAH) is predominantly caused by intracranial aneurysm rupture, which accounts for over 80% of all cases [1]. Among the remaining SAH cases with no identified aneurysm, approximately two-thirds are categorized as non-aneurysmal perimesencephalic hemorrhage (PM-NASH), whereas the other one-third arise from diverse alternative etiologies, including vascular malformations and trauma [2].

Basilar artery pseudoaneurysm (BAPA) is a distinct vascular lesion, characterized by the absence of a complete vascular wall structure. This pathological feature renders it susceptible to delayed or recurrent rupture following initial SAH [3]. Recent clinical studies have confirmed that pseudoaneurysm genesis is closely associated with 3 core pathological processes: vascular wall inflammation, hemodynamic disturbances, and endothelial injury [3,4].

These inherent pathological characteristics significantly limit the effectiveness of traditional coil embolization. Wide aneurysm necks and fragile vessel walls often lead to incomplete embolization or intraoperative rupture, further increasing the procedural risks [3]. Additionally, flow diverters (FDs) have been reported to reduce the rebleeding risk of pseudoaneurysm by reconstructing the hemodynamics of the parent artery [3]. However, the necessary long-term anti-platelet therapy may increase the risks of secondary rupture.

In this context, this report details our institutional experience with Traxcess-14 microguidewire (MicroVention)-assisted electrocoagulation for a single BAPA case, offering a reference for managing complex and refractory BAPA cases where conventional treatments are unfeasible.

CASE REPORT

A patient in their 60s was admitted to the emergency department with sudden-onset severe headache accompanied by nausea and vomiting for 4 hours. Patient had a 5-year history of hypertension, with well-controlled blood pressure through taking antihypertensive medication. The patient was neurologically intact, with a Glasgow Coma Scale score of 15, Hunt-Hess grade II, and an initial blood pressure of 181/92 mmHg.

Emergency cranial computed tomography (CT) revealed extensive and spontaneous SAH, predominantly distributed in the interpeduncular cistern, prepontine cistern, and lateral sylvian fissures, consistent with Fisher Grade 3. Subsequent computed tomography angiography (CTA) demonstrated no evidence of aneurysm, arteriovenous malformation, or dural arteriovenous fistula within the brain. On admission, the patient underwent urgent digital subtraction angiography (DSA), which also failed to identify definite aneurysms or other vascular abnormalities. Based on the integrated clinical and imaging findings, the patient was preliminarily diagnosed with PM-NASH. The patient was admitted to the neuro-intensive care unit for conservative management, including blood pressure control, anti-vasospasm therapy, pain relief, and symptomatic support. The patient was discharged on the 10th hospital day in stable condition, with scheduled close outpatient follow-up.

One month after discharge, the patient returned to our hospital for scheduled follow-up, where a comprehensive multimodal imaging evaluation was performed, including cranial CTA, high-resolution magnetic resonance vessel wall imaging (HR-VWI), and DSA. Cranial CTA revealed an ovoid space-occupying lesion located at the dorsal side of the basilar artery and anterior to the pons (Fig. 1A). In addition, HR-VWI clearly demonstrated a localized protrusion on the dorsal wall of the upper basilar artery, with annular enhancement on contrast-enhanced sequences, suggesting a vascular wall inflammatory response (Fig. 1B). For definitive diagnosis, the patient underwent DSA, which showed a tiny pseudoaneurysm (approximately 3.8 mm×4.3 mm) with an extremely narrow neck on the posterolateral wall of the upper basilar artery (Fig. 1C).

Fig. 1.

Imaging findings and interventional coagulation procedure of BAPA. (A) Cranial CTA performed 1 month after spontaneous subarachnoid hemorrhage. (B) High-resolution magnetic resonance vessel wall imaging of T1-weighted images with contrast administration reveals enhancement of the lesion (arrow). An ovoid lesion on the dorsal aspect of the basilar artery (C). The arrow indicates minimal thrombus formation at the guidewire tip after the third electrocoagulation (D), while the arrow denotes extensive thrombus formation around the guidewire after the fourth electrocoagulation (E). (F) Fifteen minutes after intravenous bolus injection of 10 mL tixofiban, angiography demonstrated resolution of the thrombus and no visualization of the BAPA. (G) Axial brain MRI sequences obtained on postoperative day 1. (H) Intracranial CTA at 6 months postoperatively. BAPA, basilar artery pseudoaneurysm; CTA, computed tomography angiography; HRA, high right anterior; AFL, anterior frontal left; PH, posterior horizontal; MRI, magnetic resonance imaging.

Following adequate informed consent regarding the potential spontaneous resolution of pseudoaneurysms, the patient refused conservative management. The patient also rejected microsurgery. Subsequently, based on the multimodal imaging data, we thought traditional coil embolization posed substantial challenges owing to the aneurysm’s tiny size and narrow neck. Furthermore, the patient’s prior episode of SAH indicated a heightened risk of rebleeding. FDs implant, which requires long-term dual antiplatelet therapy, would further increase this rebleeding risk. Consequently, endovascular electrocoagulation was selected as a salvage therapeutic option.

A Traxcess-14 microguidewire was navigated through a microcatheter to the peri-pseudoaneurysm region. The distal tip of the microguidewire was shaped into a small hook configuration to enhance its anchoring stability within the aneurysm neck. An immediate intraprocedural angiographic assessment was performed, and the images confirmed the absence of contrast agent opacification in the pseudoaneurysm sac. Subsequently, the electrocoagulation system was connected to the Solitaire stent detachment system (ev3). The therapeutic parameters were set to 4.0 V and 1.0 mA, with each electrocoagulation cycle duration of 30 seconds [5]. After the third cycle, angiography demonstrated complete obliteration of the aneurysm accompanied by minimal thrombus formation in the adjacent Traxcess-14 microguidewire (Fig. 1D). To ensure the therapeutic effect, an additional electrocoagulation cycle was administered. Post-procedural angiography revealed extensive thrombus formation surrounding the Traxcess-14 microguidewire (Fig. 1E); immediately thereafter, a 10-mL intravenous bolus of tirofiban was administered. Fifteen minutes later, repeat angiography confirmed partial dissolution of the guidewire-associated thrombus (Fig. 1F). The final angiogram verified pseudoaneurysm occlusion.

Postoperatively, the patient presented with mild facial hypoesthesia, without neurological deficits such as dysphagia or limb weakness. Brain magnetic resonance imaging (MRI) revealed scattered acute ischemic foci in the brainstem, with no radiological evidence of intracranial hemorrhage (Fig. 1G). These mild neurological symptoms resolved completely 1 week postoperatively. At the 1-month follow-up, brain MRI showed chronic ischemic foci within the pons. At 6-months, cranial CTA demonstrated resolution of the BAPA (Fig. 1H). The patient reported no residual neurological symptoms with a modified Rankin Scale score of 0.

DISCUSSION

BAPAs are frequently misdiagnosed in clinical practice, with 3 primary factors contributing to this diagnostic challenge. First, in the acute phase following hemorrhage, surrounding hematoma compression or segmental vasospasm of the parent artery may obscure the lesion, preventing adequate visualization on initial imaging. Second, a subset of BAPAs presents with partial intraluminal thrombosis or extremely small dimensions, which significantly increases the false-negative rate on standard angiographic assessments. Third, technical inconsistencies in angiographic protocols, such as suboptimal selection of acquisition phases or inappropriate setting of projection angles, may compromise the detection of subtle lesions. Notably, among BAPA cases with negative initial angiography, approximately 2–22% demonstrate detectable lesions on follow-up imaging performed 2–6 weeks later [6]. Traditional clinical protocols recommend repeat DSA for patients with unexplained SAH. However, with the rapid advancement of imaging technology, multimodal imaging follow-up strategies have become the mainstream approach for cases with negative initial DSA—offering a balance of non-invasiveness, diagnostic accuracy, and comprehensive pathological evaluation.

Among these multimodal techniques, HR-VWI stands out for its unique advantages in evaluating vascular wall pathology. Specifically, HR-VWI enables: (1) precise identification of intramural hematomas (a key pathological feature of dissecting pseudoaneurysms), with clear differentiation from luminal lesions; (2) dynamic assessment of perianeurysmal inflammatory changes (e.g., vascular wall enhancement on contrast-enhanced sequences), which aids in distinguishing pseudoaneurysms from other vascular anomalies; and (3) visualization of subtle vascular wall pathological changes (such as focal wall thickening or discontinuity) that are often missed by luminal imaging modalities (e.g., CTA or conventional DSA) [7]. This capability makes HR-VWI a critical component in the diagnostic workup of occult vascular lesions underlying unexplained SAH.

Current treatment options for BAPA are diverse, including conservation treatment, microsurgery, and interventional therapy (including coil embolization, stent-assisted embolization, and FD placement) [8]. Complete spontaneous resolution of pseudoaneurysms is rare, but it is possible. Studies indicate that specific pseudoaneurysms may follow a benign course with conservative management; observation could be considered for lesions showing reduced size and diminished blood flow on follow-up angiography [9]. However, case reports have documented re-enlargement of cerebral pseudoaneurysms after spontaneous resolution [10]. Thus, rigorous long-term follow-up is mandatory for patients under conservative treatment, even those with complete spontaneous obliteration.

Microsurgery is indicated for pseudoaneurysms following failed endovascular therapy or ruptured lesions complicated by acute hematoma with significant mass effect. Surgical options include direct clipping, suturing, wrapping-clipping, parent artery ligation, and trapping [3]. However, pseudoaneurysms lack a true vascular wall and intact neck, increasing the risk of intraoperative avulsion and bleeding. Trapping is a definitive treatment for pseudoaneurysms, with concurrent bypass performed to ensure adequate cerebral perfusion when needed. Aneurysm resection with end-to-end anastomosis represents another feasible option for select cases.

In addition, interventional embolization is an alternative therapy. The complete occlusion rate of coil embolization for wide-necked or thrombosed BAPAs is only 54–62% [11]. Standalone coil embolization may lead to early recanalization in cases of large BAPAs, often requiring secondary intervention. For small BAPAs, standalone FD placement has shown promising therapeutic effects, suggesting that FDs alone may suffice for vascular reconstruction and hemostasis in select cases [11]. These findings indicate that existing endovascular techniques still have limitations in extreme cases, highlighting the need for more aggressive or alternative therapeutic strategies.

In a clinical study of 10 patients with intracranial aneurysms, all achieved Raymond Grade 1 embolization following electrocoagulation with varying treatment durations; during 6–12 months of postoperative follow-up, no aneurysm recurrence or parent artery occlusion was observed [12]. Lu et al. [5] demonstrated that microguidewire-assisted electrocoagulation can achieve an immediate occlusion rate of 87%, though inadequate energy control may lead to complications such as vasospasm and delayed parent artery stenosis. Jiang et al. [13] further emphasized the unique value of this technique in treating intracranial perforating aneurysms with difficult microcatheter positioning, providing a novel therapeutic option for hemorrhagic lesions of small vessels. Collectively, these studies confirm that electrocoagulation treatment promotes intraluminal thrombosis in aneurysms, achieving durable occlusion outcomes. However, this therapeutic modality remains a double-edged sword. Our study identified significant brainstem ischemic lesions postoperatively, which may be attributable to thermal injury induced by electrocoagulation. Therefore, when selecting this method, the risks posed by ischemic complications must be taken into account. Endovascular microguidewire-assisted electrocoagulation may serve as a supplementary therapeutic modality for cerebral aneurysms in special condition. In addition, standardized safety parameters (e.g., optimal voltage and current) for electrocoagulation thus remain undefined, necessitating preclinical studies to establish evidence-based technical protocols.

The detailed pathophysiological mechanism of electrocoagulation-induced thrombosis remains incompletely understood, but it is hypothesized to involve 2 core processes including thrombus formation and vascular wall endothelial remodeling. (1) Electrocoagulation may induce the aggregation of negatively charged blood components (e.g., platelets, fibrinogen) within the pseudoaneurysm lumen, initiating the intrinsic coagulation cascade. (2) The electrothermal effect may accelerate thrombus formation, promote thrombus degeneration and organization (converting unstable fresh thrombi into stable fibrotic tissue), and simultaneously inhibit fibrinolysis—reducing the likelihood of thrombus recanalization. (3) Electrical stimulation may trigger a localized inflammatory response in the vascular endothelium and upregulate the release of factors such as vascular endothelial growth factor, which in turn facilitates endothelial repair and remodeling. However, the specific molecular and cellular mechanisms underlying these processes require further basic research to clarify. This case report’s single-case design limits generalizability, as the lesion features may not reflect all BAPAs. There is no comparative data to assess Traxcess-14-assisted electrocoagulation versus other treatments, and the 6-month follow-up is too short to evaluate long-term outcomes or late complications.

Traxcess-14 microguidewire-assisted endovascular electrocoagulation may serve as a therapeutic option for select intracranial pseudoaneurysms where conventional endovascular approaches and microsurgery are technically unfeasible or have failed.

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