Angiogram Negative Subarachnoid Hemorrhage Revealed as Midbasilar Perforator Pseudoaneurysm Rupture on Delayed Angiography

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J Neurointensive Care. 2025;8(2):62-66

Publication date (electronic) : 2025 October 30

doi : https://doi.org/10.32587/jnic.2025.00857

Joon Hyeoung Kim¹, Jun Soo Byun², Min Ho Kong¹, Se Youn Jang¹, Jung Hee Kim¹, Sunghoon Kim^,1

¹Department of Neurosurgery, Seoul Medical Center, Seoul, Korea

²Department of Radiology, Seoul Medical Center, Seoul, Korea

Corresponding Author: Sunghoon Kim, MD Department of Neurosurgery, Seoul Medical Center, Seoul Medical Center, 156, Sinnae-ro, Jungnang-gu, Seoul 02053, Korea Tel: +82-2-2276-7000 Fax: +82-2-2276-8595 Email: mangksh81@naver.com

Received 2025 September 11; Revised 2025 October 16; Accepted 2025 October 20.

Abstract

INTRODUCTION

Spontaneous subarachnoid hemorrhage (SAH) is a catastrophic neurological event, most often caused by the rupture of an intracranial aneurysm. Despite advances in computed tomography angiography (CTA) and transfemoral cerebral angiography (TFCA), up to one-fifth of patients present with negative initial angiographic findings, a condition referred to as angiogram-negative subarachnoid hemorrhage. For clinicians, this scenario remains a source of considerable anxiety because the risk of rebleeding persists even when no vascular lesion is initially identified. Although most perimesencephalic SAH cases are non-aneurysmal and follow a benign clinical course, diffuse bleeding patterns carry a higher likelihood of an underlying vascular lesion. Therefore, patients with diffuse angiogram-negative SAH require repeat angiography to exclude a missed aneurysm. Multiple studies have demonstrated that previously undetected aneurysms can be revealed on follow-up examinations1).

Among the rare lesions responsible for delayed detection are basilar perforator pseudoaneurysms. These lesions are exceptionally uncommon, with only a handful of cases reported worldwide, and are often missed on initial imaging owing to their small size, atypical morphology, and deep posterior circulation location1). Optimal treatment strategies remain controversial, with options ranging from conservative observation to endovascular intervention such as stent-assisted coiling or flow diversion2). Notably, when endovascular coiling is attempted, technical modifications may be necessary; in particular, partial coil deployment combined with stent support has been reported as a feasible strategy when conventional complete coil packing is unsafe or technically unachievable.

Herein, we describe a rare case of angiogram-negative subarachnoid hemorrhage in which the causative lesion—a ruptured midbasilar perforator pseudoaneurysm—was identified only on delayed TFCA. The lesion was treated with a technically modified stent-assisted coiling approach involving partial coil deployment, resulting in complete angiographic occlusion. This case highlights the diagnostic pitfalls of angiogram-negative subarachnoid hemorrhage, the necessity of follow-up imaging, and the clinical decision-making challenges in managing basilar perforator pseudoaneurysms.

CASE

A 65-year-old male with a history of hypertension and hyperlipidemia presented to the emergency department with a sudden onset of thunderclap headache. On admission, he was alert with no focal neurological deficits. Initial brain CT revealed diffuse subarachnoid hemorrhage involving the left suprasellar cistern, prepontine cistern, left ambient cistern, sylvian fissure, and interhemispheric fissure (Fig. 1A-C). CTA showed no definite aneurysm, although a subtle bulging contour at the left superior cerebellar artery origin was suspected (Fig. 1D). A diagnostic TFCA performed the same day did not identify a causative vascular lesion (Fig. 1E).

Fig. 1.

Initial imaging studies at admission. (A-C) Axial brain CT scans demonstrate diffuse subarachnoid hemorrhage involving the suprasellar, prepontine, and sylvian cisterns. (D) CTA shows no definite aneurysm or vascular abnormality. (E) TFCA also fails to identify a causative lesion, consistent with angiogram-negative subarachnoid hemorrhage at presentation.

The patient was admitted to the intensive care unit (ICU) and managed according to the aneurysmal subarachnoid hemorrhage protocol, including nimodipine administration and daily CT follow-up. Over the first week, he remained neurologically stable, and interval CT demonstrated gradual clearance of blood except for persistent prepontine cisternal hemorrhage (Fig. 2).

Fig. 2.

Serial follow-up CT scans demonstrate progressive resolution of diffuse cisternal hemorrhage, whereas persistent high-density blood remained localized in the prepontine cistern, suggesting the rupture site of the midbasilar perforator pseudoaneurysm later confirmed on angiography.

On hospital day 7, a follow-up TFCA revealed a bilobulated pseudoaneurysm (2.5 × 4 mm) with partial thrombosis arising from a lateral wall of midbasilar perforator artery (Fig. 3A). Given the lesion’s fragile morphology and risk of rebleeding, microselective angiography was performed, which confirmed the pseudosac in greater detail (Fig. 3B). Endovascular treatment was undertaken under general anesthesia. A 7-Fr Shuttle sheath was placed via the right femoral artery, and a 6-Fr Sofia intermediate catheter (MicroVention, Tustin, CA, USA) was navigated up to the V2 segment of the left vertebral artery for stable distal access. The aneurysm was catheterized using an SL-10 microcatheter (Stryker Neurovascular, Fremont, CA, USA), and a Headway 17 microcatheter (MicroVention, Tustin, CA, USA) was used for stent delivery. A small portion of a detachable platinum coil (Target Tetra 2 × 2.5 mm; Stryker Neurovascular, Fremont, CA, USA) was first deployed within the pseudoaneurysm sac to create a loose frame, followed by full deployment of an LVIS Evo braided stent (3.5 × 17 mm; MicroVention, Tustin, CA, USA) from the left posterior cerebral artery to the basilar trunk using a semi-jailing technique. Additional coil packing was carefully attempted; however, because the aneurysm wall appeared extremely fragile and resistance was encountered during coil advancement, the remaining coil was gently pushed and left partially within the stent lumen to provide internal stabilization while avoiding excessive pressure on the sac (Fig. 4A). This modified strategy allowed the coil loop to stabilize against the stent wall rather than achieve dense packing, thereby reducing the risk of rupture in the fragile pseudoaneurysm. The final angiogram confirmed complete obliteration of the pseudoaneurysm with preservation of the parent artery (Fig. 4B).

Fig. 3.

Delayed TFCA performed on hospital day 7. (A) A newly identified bilobulated pseudoaneurysm arising from a midbasilar perforator artery (arrow). (B) Microselective angiography was performed despite the procedural risk, in order to confirm a hematoma-encased pseudosac and to determine the lesion’s feasibility for therapeutic sacrifice (arrowhead).

Fig. 4.

Endovascular treatment and post-procedural imaging. (A) Stent-assisted coiling with partial coil deployment stabilizing the fragile pseudosac. (B) Final angiography demonstrates complete obliteration of the pseudoaneurysm with preservation of the parent artery. (C) Diffusion-weighted MRI after the procedure reveals an acute infarction in the left pontine region (arrow), consistent with perforator territory compromise.

Immediately after the procedure, the patient developed right-sided hemiparesis (grade 4/5). Diffusion-weighted MRI revealed an acute infarction in the left pontine region, consistent with perforator territory compromise (Fig. 4C). He was maintained on dual antiplatelet therapy and underwent intensive rehabilitation. At the 3-month follow-up, the patient had regained independence in activities of daily living and successfully returned to work, reporting only mild subjective weakness.

DISCUSSION

Angiogram-negative subarachnoid hemorrhage remains a persistent diagnostic challenge in clinical practice. Despite advances in imaging techniques, approximately 15–22% of patients with spontaneous subarachnoid hemorrhage present with no identifiable vascular lesion on initial angiography, yet the potential for rebleeding or delayed aneurysm detection remains significant1-3). Recent large-scale studies have emphasized that the bleeding pattern on initial CT is the most critical determinant for repeat angiographic evaluation. Nguyen et al. reported that 5.4% of 242 consecutive angiogram-negative subarachnoid hemorrhage patients were subsequently found to harbor vascular lesions only on follow-up angiography, all of which were associated with diffuse hemorrhage rather than the perimesencephalic type1). Similarly, Li et al. proposed a refined risk stratification system to predict delayed aneurysm detection, underscoring the necessity of tailored follow-up based on hemorrhage distribution and clinical parameters2). In line with these findings, Kang et al. suggested a practical follow-up protocol, recommending repeat angiography within 72 hours to 7 days in diffuse angiogram-negative subarachnoid hemorrhage to avoid missed aneurysms and optimize timing for intervention3). Collectively, these studies support an individualized yet proactive imaging strategy for diffuse Angiogram-negative subarachnoid hemorrhage, recognizing that the initial negative result does not exclude a vascular etiology.

Basilar perforator pseudoaneurysms are exceedingly rare, often undetectable on initial imaging due to their small caliber, atypical morphology, and deep posterior circulation location. Granja et al. conducted a systematic review, identifying only 18 cases over three decades, underscoring both the rarity and diagnostic challenges of this lesion4). Bhogal et al. described nine consecutive cases, further illustrating variable clinical outcomes after treatment and highlighting the complexity of therapeutic decision-making5). Cho et al. recently reported a domestic case in which both CTA and TFCA were negative initially, but a basilar perforator pseudoaneurysm was identified on repeat angiography three days later and successfully treated using a stent-in-stent sandwich technique6). Pathophysiologically, these pseudoaneurysms are believed to arise from focal dissection or rupture of the vasa vasorum rather than true saccular formation, resulting in a fragile blister-like wall prone to rebleeding In our case, the delayed angiographic appearance and bilobulated morphology with partial thrombosis are consistent with a dissection-related pseudoaneurysm, supporting the mechanisms proposed by Bhogal and Granja et al.

Treatment strategies for basilar perforator pseudoaneurysms remain controversial. Conservative management has been associated with favorable outcomes in selected cases; Granja’s meta-analysis reported a mortality of only 3.5% and good functional recovery (mRS 0–2) in 86.7% of patients(4). On the other hand, Elsheikh et al. presented a multicenter study of flow diverters in ruptured lesions, demonstrating 100% complete occlusion and 81% functional independence, but with ischemic complications in 28% and a long-term mortality rate of 13%7). These data suggest that while conservative treatment may be reasonable in carefully selected patients, active intervention remains a compelling option in the setting of rupture. In our patient, the pseudoaneurysm’s narrow perforator origin and extremely fragile wall made dense coil packing unsuitable because of the risk of rupture, and flow diversion was not considered feasible. Therefore, a modified stent-assisted coiling technique with partial coil deployment was selected to achieve hemodynamic stability while preserving the parent artery.

A distinctive feature of our case was the use of a modified stent-assisted coiling technique involving partial coil deployment tailored to the structural fragility of the pseudosac. Unlike conventional dense packing, which could have increased the risk of rupture, this modified approach allowed mechanical stabilization while minimizing pressure on the aneurysm wall. Although the patient developed a pontine infarction immediately after the procedure, he achieved meaningful functional recovery through rehabilitation. This outcome supports previous observations that patients with perforator infarction can still recover to mRS ≤ 2, particularly when early recognition and intensive rehabilitation are provided4,5).

In summary, this case highlights three key points. First, repeat angiography within the first week is essential in diffuse angiogram-negative subarachnoid hemorrhage, even when the initial study is negative. Second, a basilar perforator pseudoaneurysm, although exceedingly rare, should be considered a potential underlying cause. Third, a modified stent-assisted coiling technique with partial coil deployment, tailored to the fragile nature of the pseudosac, can be a feasible treatment option, offering the potential for meaningful recovery despite periprocedural complications.

CONCLUSION

Ruptured basilar perforator pseudoaneurysms, though exceptionally rare, may only be detected on delayed angiography. This case highlights the importance of follow-up angiography in diffuse angiogram-negative subarachnoid hemorrhage and demonstrates that a tailored endovascular approach can provide an effective and safe treatment option despite the fragility of the lesion.

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