Delayed mass effect following endovascular coiling of posterior inferior cerebellar artery aneurysms: Mechanism and treatment strategy: A case report

Abstract

Delayed mass effect (DME) is a rare yet significant long-term complication following endovascular coiling of intracranial aneurysms, often mimicking intracranial neoplasms and leading to diagnostic challenges. This report presents a distinctive case of DME that occurred 3 years after coiling of a posterior inferior cerebellar artery (PICA) aneurysm, characterized by a prolonged latency period, imaging findings suggestive of an evolving mass lesion, and concurrent pulmonary pathology that compounded diagnostic complexity. A 59 year-old female underwent microcatheter-assisted coiling for a PICA aneurysm. Two-year post-procedural angiographic follow-up revealed aneurysm neck recanalization. At 3 years post-embolization, organized intra-aneurysmal thrombosis resulted in a prominent peribrainstem mass effect, manifesting as progressive brainstem compression symptoms. This case highlights that DME, as a rare but serious long-term complication of aneurysm coiling, warrants heightened clinical awareness. Its management necessitates early detection and personalized treatment strategies based on a comprehensive assessment of the patient's overall condition and the specific morphological features of the aneurysm.

Introduction

PICA aneurysms represent a rare subset of intracranial aneurysm, accounting for only 0.5%-3% of all intracranial aneurysms [[1], [2], [3]]. The vessel wall of a PICA aneurysm is comparatively fragile, rendering even small aneurysms prone to rupture [4]. Notably, ruptured PICA aneurysms are associated with a significantly higher acute mortality rate compared to their anterior circulation counterparts, with a threefold greater mortality from rebleeding within 48 hours [5]. PICA aneurysms are often situated deep at the cranial base or in regions with limited surgical exposure, adjacent to the medulla oblongata and cranial nerves IX through XI. Consequently, microsurgical clipping of PICA aneurysms is constrained by a narrow operative corridor and carries risks of serious complications such as medullary and lower cranial nerve dysfunction [2,6].

Endovascular treatment (EVT) offers a less invasive alternative and has proven effective in managing patients with ruptured PICA aneurysms [7,8]. However, EVT for PICA aneurysms presents several challenges, including a relatively high recurrence rate, technical difficulties in catheter navigation due to the tortuous course and small caliber of the PICA, and the risk of compromising critical brainstem- and cerebellar-supplying perforators during embolization. Furthermore, organization of intra-aneurysmal thrombus following embolization may lead to DME, resulting in compression of adjacent neural structures. DME is a rare but significant complication after interventional embolization of PICA aneurysms. Its underlying mechanisms remain incompletely understood but may involve thrombus organization, inflammatory responses, and local tissue remodeling. DME can cause brainstem compression, hydrocephalus, or cranial nerve dysfunction, severely impacting patient prognosis. Therefore, early identification and intervention are crucial, and investigating its pathogenesis along with developing prevention and management strategies holds considerable clinical significance.

Case presentation

A 59-year-old female presented more than 3 years ago with headache and intermittent numbness of the right limb without an obvious cause. Evaluation at a local hospital suggested a left PICA aneurysm. Her neurological status was intact at that time (Glasgow Coma Scale (GCS) score 15, National Institutes of Health Stroke Scale score 0, modified Rankin Scale score 0). Complete digital subtraction angiography (DSA) revealed a slender right vertebral artery and a saccular aneurysm arising from the left PICA, measuring approximately 6.00 mm × 4.86 mm × 6.28 mm with a neck width of 3.91 mm. Multiple branch vessels were visualized within the aneurysm sac (Fig. 1A-C).

Fig. 1.

Therapeutic angiographic sequence. (A and B) Lateral and anteroposterior digital subtraction angiography projections via left vertebral artery injection. (C) Magnified subtracted view demonstrating a saccular aneurysm (6.00×4.86×6.28 mm) originating from the proximal PICA with 3.91 mm neck width. (D) Immediate post-embolization angiography confirms complete aneurysm occlusion (Raymond-Roy Class I) with preserved PICA patency following microcatheter-assisted coiling. Anatomical labels: AN, aneurysm; BA, basilar artery; PICA, posterior inferior cerebellar artery; VA, vertebral artery.

The procedure was performed with the patient under general anesthesia. Intraoperative DSA confirmed the aneurysm's location at the proximal segment of the left PICA. Using a triaxial system, a Synchro 0.014 microwire was navigated to guide an SL-10 microcatheter into the aneurysm cavity. A second SL-10 microcatheter was positioned distally in the parent PICA to protect the vessel during embolization. The aneurysm was subsequently packed densely with detachable platinum coils. Post-embolization angiography demonstrated complete occlusion of the aneurysm with preserved patency of the parent artery (Fig. 1D).

At the 2-year angiographic follow-up, morphological evolution with neck recanalization of the previously coiled left PICA aneurysm was observed (Fig. 2A and B). Given the minimal extent of recanalization and the absence of symptoms, the patient declined any further intervention at that time.

Fig. 2.

Follow-up DSA imaging. (A and B) Two-year post-embolization DSA images demonstrate recurrent neck filling at the posterior inferior cerebellar artery origin (arrowheads), indicating aneurysm recanalization. (C-D) Three-year follow-up DSA confirms persistent neck recanalization (arrowheads) with stable coil configuration (*). Anatomical labels: AN, aneurysm; BA, basilar artery; Coil, embolization coils; PICA, posterior inferior cerebellar artery; VA, vertebral artery.

In the third year following the initial embolization, the patient was readmitted due to the acute onset of right-sided hemiparesis and ipsilateral facial paralysis. Neurological examination upon admission revealed a GCS score of 15 with normal verbal response. Cranial nerve assessment showed symmetric forehead wrinkles and nasolabial folds but a deviation of the right oral commissure. Motor examination documented Medical Research Council grade 1/5 strength in the right extremities, contrasting with full strength (5/5) on the left side. Muscle tone was normal, and no pathological reflexes were elicited.

Imaging reevaluation: Confirmatory DSA revealed persistent neck recanalization at the site of the treated aneurysm (Fig. 2C-D). Subsequent contrast-enhanced cranial computed tomography (CT) and magnetic resonance imaging (MRI) identified a mass lesion in the pontomedullary region. This lesion caused significant deformation of the brainstem and compression of the fourth ventricle, resulting in obstructive hydrocephalus accompanied by periventricular interstitial edema. On T1-weighted post-contrast sequences, the lesion demonstrated peripheral enhancement and appeared contiguous with the origin of the left PICA (Fig. 3). Concurrent thoracic CT demonstrated a rounded mass (2.1 × 3.4 cm) in the right upper lobe associated with hilar and mediastinal lymphadenopathy, suggestive of a neoplastic process. Additionally, patchy opacities with heterogeneous density in the apical segment of the right upper lobe raised the possibility of fungal infection, with further infectious infiltrates noted in both lower lobes (Fig. 4).

Fig. 3.

Neuroimaging Findings. (A, E) Contrast-enhanced cranial CT series demonstrate a 0.6 cm nodular protrusion at the left posterior inferior cerebellar artery origin, surrounded by a heterogeneous hyperdense lesion (maximum cross-section: 3.3×2.4 cm). Significant mass effect is evidenced by brainstem deformation and fourth ventricular compression, resulting in upstream ventricular dilatation, Evans >0.3. (B-D, F-H) Multiplanar contrast-enhanced MRI sequences reveal pontine and medullary expansion containing a heterogeneous signal intensity mass (3.2×2.5 cm in axial plane) with peripheral edema. A 0.8×0.6 cm intensely enhancing nodular focus is observed at the lesion's left anterior margin. The inferior fourth ventricular compression progresses to rostral ventricular system dilation, including both lateral and third ventricles.

Fig. 4.

CT-CHEST. (A-D) 2.1×3.4 cm irregular mass in right upper lobe anterior segment with pleural retraction. Apical segment heterogeneous opacity containing bronchiectasis and cavitation (intracavitary soft tissue nodule). Bilateral lower lobe-predominant infectious infiltrates. Bilateral pleural thickening (right > left) with right interlobar fissure effusion.

Management and clinical course: Based on the clinical presentation, prior surgical history, and comprehensive imaging findings, the pontomedullary mass was determined not to be a neoplasm. It was diagnosed as an organized thrombus within the previously coiled PICA aneurysm, exerting a DME. Despite the confirmed aneurysm recanalization, the presence of a concurrent pulmonary mass (suspected malignancy), severe pulmonary infection, and type II respiratory failure rendered the patient at prohibitively high risk for any surgical or endovascular re-intervention. Following a multidisciplinary consultation, the patient's family opted for conservative management. Supportive treatment, including osmotic therapy with mannitol for intracranial pressure reduction and a short course of low-dose corticosteroids, was administered. The patient's neurological symptoms showed improvement, and she was discharged in a stable condition.

Discussion

Anatomy of posterior inferior cerebellar artery and characteristics of PICA aneurysms

The PICA represents the most anatomically complex, tortuous, and variable cerebellar artery, originating from the vertebral artery to supply critical regions of the cerebellum and medulla oblongata [9,10]. According to the anatomical relationship between PICA and medulla oblongata and cerebellum, it was divided into 5 segments: anterior medulla oblongata (p1), lateral medulla oblongata (p2), tonsil medulla oblongata (p3), membranous tonsil (p4) and cortical segment (p5) [[11], [12], [13]]. Some scholars have defined the proximal part of p1, p2, and p3 segments as the proximal part of PICA, while the remaining parts are defined as the distal part of PICA [4]. PICA aneurysms are relatively uncommon, accounting for approximately 0.5%-3% of all intracranial aneurysms [14,15]. These aneurysms may arise from any segment of the PICA, with the majority located at the vertebral artery–PICA junction, while only a minority originate from the PICA trunk itself [16,17].

Both microsurgery and EVT demonstrate remain viable options for PICA aneurysms. Compared with EVT, the incidence of posterior cranial nerve paralysis caused by microsurgery is higher (22.7% vs 0.4%) [18]. However, the recurrence rate of PICA aneurysms treated with EVT was higher. The recurrence rate of patients receiving EVT was 8.1%, while the recurrence rate of aneurysms in the surgical group was 1.1% [19]. Nationwide SOS registry data from Switzerland corroborate EVT's clinical utility, with 55.4% of ruptured PICA aneurysms successfully managed endovascularly, achieving favorable outcomes at 1-year follow-up [20].

Ideally, the purpose of treatment is to completely embolize the PICA aneurysm while preserving the parent and perforating arteries [2,7]. However, PICA's inherent anatomical complexity—including vessel tortuosity, small caliber, variable VA-PICA angles, and diameter discrepancies—poses significant challenges for endovascular techniques. These limitations often preclude the use of stent- or balloon-assisted coiling [21]. Luckily, microcatheter-assisted coil embolization can be used as an effective treatment strategy to preserve the distal end of the posterior inferior cerebellar artery in PICA aneurysms. It can achieve complete occlusion of aneurysms while ensuring the patency of the distal blood flow of PICA, and has high clinical application value [22]. This case was managed with a dual-microcatheter coiling technique. Coils were delivered via an SL-10 microcatheter in the aneurysm sac, while a second SL-10 microcatheter positioned distal to the aneurysm neck protected the parent PICA and prevented coil prolusion. Post-embolization angiography confirmed parent artery patency. Regrettably, 2-year follow-up DSA revealed aneurysm neck recanalization. Subsequent intra-aneurysmal thrombosis and thrombus organization within the following year induced peribrainstem mass effect.

Investigation into mechanisms of delayed mass effect

DME refers to a clinical phenomenon where initially treated intracranial lesions (such as aneurysms, abscesses, or tumors) subsequently develop progressive compression on adjacent neural structures due to volume expansion, hemorrhage, or perilesional edema. Literature reports indicate that large or giant aneurysms (>18 mm) are more prone to DME, with an incidence reaching 30.0% in patients with aneurysms exceeding 18 mm, where aneurysm size >18 mm serves as an independent risk factor for aggravated mass effect [23]. Patients developing delayed progressive mass effect after endovascular embolization often exhibit poor prognoses, frequently requiring life-saving decompressive surgery [24]. A 20-year follow-up study of basilar tip aneurysms post-embolization revealed that most late-term deaths resulted from progressive mass effect rather than rebleeding events [25].

The pathophysiological mechanisms of DME are complex, involving interactions among inflammatory responses, thrombosis, thrombus organization, altered vascular permeability, and mechanical compression [24,26]. Thrombosis in the aneurysm cavity after embolization is the initial link of the mass effect [27,28]. During early thrombus formation, clots composed of red blood cells and fibrin are gradually replaced by fibroblasts, forming dense connective tissue through thrombus organization. Dense embolization may increase intra-aneurysmal pressure, promoting thrombus organization. This process can temporarily enlarge the aneurysm sac, compressing surrounding structures and worsening mass effect [[29], [30], [31]]. Potential pathological mechanisms of DME may also involve oxidative stress and complement system activation. Inflammatory mediators (eg, IL-6, TNF-α) released during these processes trigger local inflammation. Within 1 to 2 weeks post-coiling, most patients exhibit infiltration of inflammatory cells, macrophages, and fibroblasts. These changes disrupt blood-brain barrier integrity, increase vascular permeability, and promote cerebral edema formation [24,29,32]. Additionally, mechanical irritation from coils on the aneurysm wall may induce localized vasospasm or microcirculatory impairment, further exacerbating mass effect.

Diagnosis and management of delayed mass effect following endovascular embolization of intracranial aneurysms

DME presents with diverse clinical manifestations depending on lesion location and severity. Common symptoms include progressive focal neurological deficits (cranial neuropathies, limb weakness, hemiparesis, aphasia), elevated intracranial pressure (headache, nausea, vomiting), seizures, and consciousness impairment. Posterior circulation aneurysms may induce brainstem compression, hydrocephalus, or cranial nerve dysfunction, with severe cases progressing to cerebral herniation [30]. In this case, the patient developed right-sided hemiparesis and facial palsy 3 years post-embolization of a proximal PICA aneurysm. Brain MRI revealed a left-sided brainstem mass lesion with fourth ventricular compression, obstructive hydrocephalus, and periventricular interstitial edema. Contrast-enhanced cranial CT and MRI both demonstrate intracranial space-occupying lesions, which are often easily misdiagnosed as intracranial tumors, and should be distinguished from intracranial tumors (Table 1).

Table 1.

Clinical timeline of the case.

Time point	Key findings	Intervention
Initial visit	Headache and right limb numbness; DSA confirmed a left PICA aneurysm.	Coil embolization of the left PICA aneurysm using a dual-microcatheter technique. Immediate post-procedural angiography confirmed complete aneurysm occlusion.
2 y post-procedure	Follow-up DSA revealed neck recanalization of the aneurysm.	Surveillance observation without further intervention.
3 y post-procedure	Acute onset of right hemiparesis and facial palsy; Cranial CT/MRI indicated a brainstem mass with secondary obstructive hydrocephalus; Chest CT showed a right upper lobe mass, accompanied by severe pulmonary infection and respiratory failure; Repeat DSA confirmed aneurysm recanalization.	The family opted for conservative management. Treatment included mannitol for dehydration and a short course of low-dose corticosteroids. The patient was discharged after stabilization.

Intracranial tumors typically exhibit marked mass effect with significant perilesional edema, demonstrating irregular/homogeneous/ring-like enhancement without parent artery visualization. While digital subtraction angiography remains the diagnostic gold standard, complete thrombosis may occlude the parent artery, preventing distal vascular filling, and are often misdiagnosed as intracranial tumors [33]. Professor You et al. [34] reported a 9-year-old child with a thrombosed giant PICA aneurysm mimicking an intracranial tumor. Preoperative MRI identified a well-defined irregular mass ventral to the pons, initially diagnosed as an epidermoid cyst, which was later confirmed via suboccipital retrosigmoid approach to originate from the proximal PICA. Recently, some scholars reported a case of a gourd-shaped posterior fossa mass. During the operation, it was found that the lesion originated from the distal end of the PICA. Intraoperative exploration revealed organized thrombus with hemosiderin-laden macrophages, with histopathological confirmation of true aneurysm diagnosis postoperatively [35].

Currently, there is no standardized protocol for the clinical management of DME; however, early recognition and personalized intervention are crucial. The formulation of management strategies should follow a systematic decision‑making process. First, a comprehensive assessment is required, integrating neuroimaging findings (to clarify the degree of mass effect, hydrocephalus, and aneurysm status) with an evaluation of the patient's systemic condition (with particular attention to comorbidities such as infection and organ function). Second, treatment options should be stratified: for asymptomatic or mildly symptomatic and stable patients, conservative management may be chosen, including the use of osmotic diuretics (eg, mannitol) to reduce edema and short‑term administration of corticosteroids (eg, dexamethasone) to suppress the inflammatory response and alleviate the mass effect [23,25]. However, more active intervention should be considered under the following circumstances: 1) symptoms progress from moderate to severe; 2) progressive brainstem compression or obstructive hydrocephalus is present (eg, increasing Evans index); 3) definite neck recanalization or recurrence of the aneurysm is identified. Intervention measures include (and may be used alone or in combination as appropriate): a) Endovascular retreatment: for recurrent aneurysms, options include repeat coiling, stent‑assisted coiling, or flow‑diverter (FD) implantation, aiming both to occlude the aneurysm and to mitigate the mass effect caused by intra‑aneurysmal thrombosis; b) Cerebrospinal fluid diversion: for patients with hydrocephalus, ventriculoperitoneal or lumboperitoneal shunting may be considered to lower intracranial pressure; c) Surgical decompression: for severe mass effect refractory to medical therapy, or when EVT is not feasible, posterior fossa decompression serves as a last‑resort measure to preserve neurological function. In the present case, due to concomitant severe pulmonary fungal infection and respiratory failure (posing an extremely high surgical risk) and in accordance with family preference, conservative management was chosen despite the presence of brainstem compression, resulting in short-term symptomatic improvement.

If patients can tolerate surgery, microsurgery is still an effective treatment for the mass effect caused by recurrent aneurysms after interventional embolization, but it still faces the challenge of narrow surgical operation space [36,37]. FD may be a safe and feasible treatment option for recurrent PICA aneurysms after coil embolization [3,9,38]. Only coil embolization may be difficult to achieve complete remission due to the space occupying effect caused by thrombosis in the aneurysm cavity after embolization [39]. FD is effective in relieving compression symptoms due to large and giant intracranial aneurysms and help to reduce the mass effect [40]. In addition, the use of FD combined with loose coil packing may help to reduce the mass effect caused by large or giant intracranial aneurysms [26].

Conclusion

DME is a rare complication following the endovascular coiling of intracranial aneurysms, which can be misdiagnosed as a tumor. Therefore, the treatment of delayed mass effect after PICA aneurysm recurrence should be based on patient characteristics, aneurysm structure, severity, and surgeon experience to develop a personalized treatment plan [41].

Authors contributions

All authors contributed to the preparation of this work.

Patient consent

Written informed consent was obtained from the patient for publication of this case report.