Progressive thrombosed pseudoaneurysm following transarterial balloon embolization in traumatic carotid-cavernous fistula: From silent lesion to symptomatic mass

Abstract

Background:

Pseudoaneurysm formation is a known but often underrecognized long-term complication following balloon embolization for traumatic carotid-cavernous fistula (TCCF). While many pseudoaneurysms remain asymptomatic, progressive enlargement and thrombosis may lead to mass effect and delayed neurological manifestations, including seizures and visual disturbances.

Case Description:

We report the case of a 33-year-old man who presented with new-onset generalized tonic–clonic seizure and binocular visual disturbances 14 years after undergoing transarterial detachable balloon embolization for TCCF. Brain magnetic resonance imaging revealed a large, partially thrombosed pseudoaneurysm arising from the cavernous segment of the internal carotid artery, extending into the suprasellar region with compression of the optic chiasm and adjacent frontal lobe. Humphrey visual field testing demonstrated bitemporal hemianopia. The patient underwent successful endovascular stent-assisted coiling. Post-treatment follow-up showed marked improvement in visual fields and complete seizure resolution, with no evidence of aneurysmal recurrence at 3 years.

Conclusion:

This case highlights the importance of long-term surveillance following balloon embolization for TCCF. Delayed pseudoaneurysm growth may lead to significant neurological deficits years after initial treatment. Early recognition and appropriate endovascular intervention are essential to prevent irreversible complications and optimize patient outcomes.

INTRODUCTION

Traumatic carotid-cavernous fistula (TCCF) is a high-flow direct arteriovenous communication between the cavernous segment of internal carotid artery (ICA) and cavernous sinus, most commonly resulting from blunt craniofacial trauma. Clinical manifestations typically include pulsatile proptosis, conjunctival chemosis, orbital bruit, cranial nerve palsies, and, in severe cases, vision loss or cerebral venous hypertension due to cortical venous reflux.[9,10]

Endovascular treatment has largely supplanted surgical approaches, with transarterial balloon embolization using detachable latex balloons historically being a mainstay in the management of direct TCCFs. This technique offers effective occlusion of the fistulous tract while preserving flow through the parent artery. Despite the widespread adoption of coils and flow diverters in recent years, detachable balloon embolization continues to be utilized in certain regions due to its simplicity and effectiveness.[11]

While the procedure is generally safe and effective, pseudoaneurysm formation is a common but usually benign long-term outcome following detachable balloon treatment for TCCF. These pseudoaneurysms arise at the site of arterial wall injury or balloon detachment and may remain stable and asymptomatic for many years.[25] However, progressive enlargement can occur, potentially leading to mass effect, thromboembolic events, or delayed neurological complications.[5]

We present a rare case of a delayed symptomatic cavernous ICA pseudoaneurysm, identified 14 years after successful transarterial balloon embolization for TCCF. Initially, a silent, thrombosed lesion, the pseudoaneurysm enlarged over time and eventually presented with new-onset seizure and visual field disturbance. The lesion was successfully treated using stent-assisted coiling, achieving complete obliteration. This case underscores the importance of long-term imaging surveillance following balloon embolization, even in asymptomatic patients, and highlights the utility of modern endovascular techniques in addressing delayed complications.

CASE REPORT

A 33-year-old man was referred to our institute after experiencing a 5-min episode of generalized tonic-clonic seizure while watching television. He was initially evaluated at a local hospital, where he received anticonvulsant therapy. In addition, he reported complaints of diplopia. Brain magnetic resonance imaging (MRI) was performed under suspicion of a neoplastic process, prompting referral to our center for further evaluation.

One month before presentation, the patient sustained a fall and struck the right side of his head on the floor, resulting in transient loss of consciousness. He subsequently developed blurred vision in the right eye but did not seek medical attention at that time.

At the age of 15, he had suffered a severe traumatic brain injury following a motorcycle collision with an electric pole, resulting in fractures of the left orbital rim and mandible. He underwent internal fixation and required a 2-month hospital stay, after which he fully recovered.

At the age of 19, the patient developed progressive left eye proptosis and conjunctival injection. He was diagnosed with a direct TCCF and underwent transarterial balloon embolization at another university hospital, resulting in complete resolution of symptoms. Follow-up MRI and magnetic resonance angiography (MRA) performed 8 years post-embolization revealed a partially thrombosed pseudoaneurysm arising from the inferomedial wall of the posterior genu of the cavernous segment of the left ICA, occupying the sellar fossa [Figures 1 and 2]. The patient was asymptomatic at that time and was subsequently lost to follow-up.

Figure 1:

Magnetic resonance imaging of the brain obtained 8 years after balloon embolization. (a-c) Sequential axial T2-weighted, (d) T1-weighted, (e) T1-weighted with contrast, and (f) coronal T1-weighted with contrast images demonstrate a well-defined lesion with a mildly lobulated contour and heterogeneous enhancement. The lesion exhibits mixed T1 and T2 iso-, hypo-, and hyperintense signals and is located in the sellar fossa, contiguous with the left cavernous segment of the internal carotid artery, suggestive of a partially thrombosed pseudoaneurysm.

Figure 2:

Oblique view of maximum intensity projection time-of-flight magnetic resonance angiography of the left internal carotid artery (ICA) demonstrates a large pseudoaneurysm at the inferomedial wall of the posterior genu of the cavernous segment of the left ICA.

At our institute, 14 years after the initial embolization, neurological examination revealed a fully conscious and alert patient with no motor or sensory deficits. Ophthalmological evaluation demonstrated a visual acuity (VA) of 20/200 in the right eye, uncorrected by pinhole, with a pale optic disc and a positive relative afferent pupillary defect. Intraocular pressure (IOP) was 13.1 mmHg. A right lateral rectus palsy was noted. The left eye had a VA of 20/20, normal optic disc, and IOP of 14.1 mmHg. Humphrey visual field testing revealed incongruous bitemporal hemianopia [Figure 3]. Repeat MRI showed interval enlargement of the partially thrombosed cavernous ICA pseudoaneurysm, which now extended superiorly into the suprasellar cistern, with expansion of the sellar fossa [Figure 4].

Figure 3:

Humphrey visual field 30-2 perimetry charts showing incongruous bitemporal hemianopia. (a) Left eye. (b) Right eye.

Figure 4:

Magnetic resonance imaging of the brain obtained 14 years after balloon embolization. (a-c) Sequential axial T2-weighted, (d) T1-weighted, (e) T1-weighted with contrast, and (f) coronal T1-weighted with contrast images demonstrate an overall increase in size of the pre-existing partially thrombosed pseudoaneurysm of the cavernous segment of the left internal carotid artery. The lesion now occupies an enlarged sellar fossa and extends into the suprasellar region.

Digital subtraction angiography and angiographic computed tomography with maximum intensity projection reconstructions confirmed a large, wide-neck pseudoaneurysm originating from the inferomedial wall of the posterior genu of the left cavernous ICA, projecting medially and compressing the optic chiasm. Upward displacement of the bilateral A1 and A2 segments of the anterior cerebral arteries was evident. Delayed contrast stasis and incomplete filling within the lesion suggested partial thrombosis [Figures 5 and 6].

Figure 5:

Cerebral angiography obtained 14 years after balloon embolization. (a-d) Anteroposterior and (e-h) lateral views of the left internal carotid artery (ICA) injection during arterial to venous phases demonstrate a large pseudoaneurysm at the inferomedial wall of the posterior genu of the cavernous segment of the left ICA. Incomplete contrast filling within the pseudoaneurysm and contrast stasis are observed, suggesting partial thrombosis.

Figure 6:

(a) Axial, (b) coronal, and (c) sagittal maximum intensity projection reformatted images from angiographic computed tomography of the internal carotid artery (ICA) clearly illustrate a large pseudoaneurysm at the inferomedial wall of the posterior genu of the cavernous segment of the left ICA.

The patient underwent endovascular treatment under general anesthesia following systemic heparinization and loading doses of 300 mg clopidogrel and 300 mg aspirin administered through a nasogastric tube. A stent-assisted coiling procedure was performed through a transarterial approach, achieving complete obliteration of the pseudoaneurysm [Figure 7]. An Enterprise stent (Codman Neurovascular, Raynham, MA, USA) was deployed across the aneurysm neck, with additional packing using Axium coils (Medtronic, Minneapolis, MN, USA) and Target coils (Stryker Neurovascular, Fremont, CA, USA).

Figure 7:

Cerebral angiography following stent-assisted coiling. (a) Anteroposterior, (b) lateral, (c) oblique, and (d) 3D reconstruction images of the left internal carotid artery reveal complete obliteration of the pseudoaneurysm.

Postoperatively, the patient reported gradual improvement in his visual field defect. At the 2-month follow-up, his right eye VA was 20/20 with full extraocular movements. Repeat Humphrey visual field 30-2 perimetry demonstrated marked improvement in both eyes [Figure 8]. At the 3-year follow-up, annual MRA showed no recurrence of the aneurysm. The patient remained seizure-free, and antiepileptic medication was successfully discontinued 1 year after embolization.

Figure 8:

Humphrey visual field 30-2 perimetry charts obtained 2 months after endovascular treatment, demonstrating marked improvement in the visual fields. (a) Left eye. (b) Right eye.

DISCUSSION

Partially thrombosed pseudoaneurysm formation in TCCF

TCCFs treated with transarterial detachable balloon embolization can result in pseudoaneurysm formation as a long-term sequela.[25] The pathophysiology likely involves balloon deflation, migration, or direct trauma to the arterial wall, all of which may weaken the vessel and lead to delayed pseudoaneurysm formation.[5] A large single-center experience recently reported a pseudoaneurysm rate of over 67% following balloon treatment for TCCF. Pseudoaneurysm development after detachable balloon embolization is typically regarded as a benign consequence and is frequently asymptomatic.[11] Partially thrombosed intracranial aneurysms are a distinct and complex vascular entity, typically observed in large or giant aneurysms. These lesions are characterized by the formation of an intraluminal thrombus, which contributes to progressive aneurysmal growth, structural wall remodeling, and diverse clinical manifestations. In contrast to typical saccular aneurysms that often present with acute rupture, partially thrombosed aneurysms tend to follow a more chronic and indolent course. Symptoms are commonly related to mass effect or thromboembolic complications rather than hemorrhage.[2,8,13]

Although spontaneous resolution of large, partially thrombosed cerebral aneurysms has occasionally been reported, it remains an uncommon outcome.[12] The presence of thrombus may stabilize the aneurysm by promoting fibrosis and wall thickening, or alternatively, may lead to distal embolization and further aneurysmal expansion.[2,21] Due to their variable clinical behavior and potential for neurological compromise, these aneurysms require careful long-term imaging surveillance and individualized therapeutic strategies.

Seizure associated with large partially thrombosed pseudoaneurysms

Epileptic seizures are a rare but clinically significant manifestation of cerebral aneurysms. While seizures are commonly associated with structural brain lesions such as tumors, vascular malformations, or cortical scarring, their occurrence due to unruptured or partially thrombosed aneurysms is relatively uncommon. However, several case reports and clinical observations suggest that cerebral aneurysms, particularly those located near cortical structures, can provoke epileptiform activity through a variety of mechanisms.[23,24]

One commonly proposed mechanism is direct irritation or compression of adjacent brain parenchyma. Aneurysms that project toward the medial temporal lobe or basal frontal areas may exert chronic mass effect on surrounding cortical tissue. This can result in localized gliosis, neuronal irritation, or ischemia, thereby forming an epileptogenic focus. In addition, repeated microhemorrhages or deposition of blood breakdown products may promote long-term cortical hyperexcitability.[7,14]

In this case, the patient’s seizure was most likely precipitated by mass effect and chronic cortical irritation involving the basal frontal region, resulting from progressive thrombosis and enlargement of a large cavernous pseudoaneurysm. The gradual expansion of the aneurysmal sac may have exerted pressure on adjacent frontal lobe structures, generating a zone of cortical hyperexcitability and increased susceptibility to epileptogenesis. This phenomenon is particularly relevant given the delayed onset of seizure activity occurring more than a decade after the original TCCF was treated with transarterial detachable balloon embolization.

Although seizures are an uncommon manifestation of unruptured aneurysms, they should be considered in the differential diagnosis of new-onset focal seizures, especially in patients without a prior seizure history but with known vascular abnormalities. In our patient, the delayed clinical presentation suggests that the long-term evolution of a pseudoaneurysm, including intraluminal thrombosis and progressive expansion, may give rise to entirely new neurological symptoms distinct from the initial fistula-related signs. This highlights the importance of extended surveillance and radiological follow-up in patients with partially thrombosed aneurysms, particularly when located near eloquent or seizure-prone cortical regions.

Visual field deficits secondary to aneurysmal compression

Visual field deficits are a recognized clinical manifestation in patients with large or partially thrombosed intracranial aneurysms, particularly when the lesions are located in anatomically critical regions such as the paraclinoid, suprasellar, or posterior communicating artery territories. The primary mechanism involves mass effect on the visual pathways, including the optic nerve, chiasm, and tract, resulting in compressive optic neuropathy.[4,6,8] Aneurysms arising from the supraclinoid segment of the ICA or from the anterior communicating artery often exert direct mechanical pressure on the visual apparatus, as extensively documented in clinical literature.[16] In certain cases, asymmetric thrombus accumulation may distort the aneurysm’s geometry and alter the axis of compression.[1]

The pathophysiology underlying visual loss in these aneurysms is multifactorial. Progressive mural thrombosis increases the pulsatile mass effect, which can chronically compress surrounding optic structures. This sustained compression may lead to demyelination, ischemia, or axonal injury, potentially resulting in irreversible visual loss if intervention is delayed. The pattern of visual field loss may offer diagnostic clues: for example, bitemporal hemianopia suggests chiasmal involvement, whereas monocular deficits point toward pre-chiasmatic compression.[8,15]

In our case, the large, partially thrombosed pseudoaneurysm of the cavernous ICA demonstrated suprasellar extension, exerting direct mass effect on the optic chiasm. This anatomical relationship provides a plausible explanation for the patient’s visual disturbance and underscores the importance of early detection and tailored intervention in such lesions.

Management strategies for symptomatic cavernous pseudoaneurysms

The management of symptomatic pseudoaneurysms following balloon embolization for TCCFs requires a personalized approach based on lesion morphology, clinical presentation, and the potential for progression. Although spontaneous resolution of pseudoaneurysms has been reported, it remains rare and unpredictable.[17] Conservative observation may be appropriate in stable, asymptomatic cases. However, when imaging reveals enlargement, partial thrombosis, or the emergence of new neurological symptoms, active intervention is warranted. Available endovascular strategies include coiling, stent-assisted coiling, and flow diversion. Stent-assisted coiling is particularly advantageous for wide-necked aneurysms, as it provides mechanical support and promotes thrombosis while preserving parent vessel integrity. Both stent-assisted coiling and flow-diverting stents require long-term dual-antiplatelet therapy to mitigate thrombotic risks.[3,8,18]

Visual disturbances caused by aneurysmal mass effect present a distinct therapeutic challenge. Endovascular procedures may not result in immediate improvement, and visual symptoms may initially worsen due to thrombus expansion or localized inflammatory changes.[19] Nevertheless, long-term outcomes indicate that early decompression can stabilize or improve visual function, particularly when the optic pathways are not yet irreversibly damaged.[8]

Surgical treatment, though less commonly employed today, remains a key option in carefully selected cases, especially when endovascular interventions are not viable, have failed, or are unable to relieve mass effect.[21] Microsurgical approaches, such as direct clipping, thrombectomy, or aneurysm trapping with bypass, may be suitable for giant or partially thrombosed aneurysms that are associated with progressive visual loss or cranial neuropathies.[15,16] Surgery enables direct thrombus evacuation and immediate decompression of adjacent neural structures, which may be critical for patients with rapidly worsening neurological symptoms.[13] However, cavernous sinus aneurysms present substantial technical difficulties due to their deep location and proximity to vital neurovascular structures, including cranial nerves III to VI and the ICA.[10]

Intracranial pseudoaneurysms pose additional surgical challenges due to their friable walls and broad or ill-defined necks, which make direct clipping or repair particularly risky.[21] Unlike saccular aneurysms exerting mass effect over the anterior optic apparatus, which can often be treated effectively with microsurgical clipping to achieve both lesion exclusion and decompression, pseudoaneurysms frequently lack clear anatomical planes for safe manipulation.[22] Consequently, surgery is typically reserved for patients whose symptoms continue to progress despite endovascular therapy or in whom prior treatment has failed. A multidisciplinary team approach is essential for these complex cases to balance surgical risks with the potential benefits of complete lesion exclusion and symptom relief.[20]

Recent technological advancements have expanded the treatment arsenal for these difficult aneurysms. Flow-diverting stents have emerged as a valuable alternative, particularly in cases involving fusiform, dissecting, or morphologically complex pseudoaneurysms where coiling is not practical. These devices promote thrombosis within the aneurysm sac while simultaneously reconstructing the parent artery, eliminating the need for direct aneurysm access. Studies have shown that flow diverters are effective in achieving long-term aneurysm occlusion and arterial remodeling, especially for lesions in the cavernous or supraclinoid segments of the ICA.[26] Flow diversion leads to gradual thrombosis and sac shrinkage, reducing mass effect on surrounding structures such as the optic chiasm and cranial nerves. Although decompression is not immediate, several clinical reports have demonstrated significant improvement in neurological symptoms over time, supporting the utility of flow diverters in compressive aneurysms.[22]

In the present case, stent-assisted coiling provided a safe and effective treatment, resulting in complete aneurysm occlusion, resolution of seizures, and significant improvement in visual field deficits. This underscores the potential of timely endovascular intervention to reverse or prevent neurological deterioration in patients with delayed complications after TCCF treatment. Importantly, at the time of intervention, flow diverters were not available at our institution, precluding their consideration as a primary therapeutic option. This further highlights the importance of individualized treatment planning based on institutional resources and patient-specific factors.

CONCLUSION

This case emphasizes the importance of long-term imaging follow-up in patients treated with balloon embolization for TCCF. Although pseudoaneurysm formation is a recognized consequence of this procedure, its progressive enlargement can remain clinically silent for years before manifesting with serious neurological symptoms. In our patient, a large, partially thrombosed pseudoaneurysm of the cavernous ICA extended into the suprasellar space, compressing the optic chiasm and adjacent basal frontal cortex. This resulted in delayed-onset seizures and visual field deficits, underscoring the potential for evolving complications even long after initial treatment.

Effective management requires a multidisciplinary team including neurologist, ophthalmologist, and neurointerventionist to ensure accurate diagnosis and timely intervention. Modern endovascular techniques, such as stent-assisted coiling and flow diversion, offer promising therapeutic options for symptomatic pseudoaneurysms with complex morphology. Clinicians should remain vigilant for delayed presentations in patients with a history of TCCF, especially those who develop new focal neurological symptoms or visual disturbances. Early detection and tailored treatment can significantly improve long-term outcomes.

Ethical approval:

The Institutional Review Board approval is not required.

Declaration of patient consent:

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship:

Nil.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

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