Delayed thrombosis of a ruptured anterior spinal artery aneurysm after prolonged morphological stability: illustrative case

Abstract

BACKGROUND

Isolated anterior spinal artery (ASA) aneurysms are rare vascular lesions with heterogeneous morphologies and clinical behaviors. Spontaneous regression has been reported in approximately half of conservatively managed cases and typically occurs within the early months after diagnosis. However, delayed thrombosis after prolonged morphological stability is rare.

OBSERVATIONS

A 75-year-old man presented with subarachnoid hemorrhage caused by a 3-mm ruptured ASA aneurysm at the C3 level. Conservative management was initially selected because of his poor neurological status. Eleven months after diagnosis, selective microcatheter angiography demonstrated unchanged aneurysm morphology without interval growth or thrombosis. No angiographic features suggesting arterial dissection or associated vascular pathology were identified. Four weeks later, at planned embolization, repeat angiography demonstrated complete absence of aneurysmal filling with preserved parent artery continuity, consistent with isolated aneurysm sac thrombosis. No intervention was performed. Follow-up imaging confirmed persistent occlusion without recanalization.

LESSONS

Delayed thrombosis can occur in ruptured ASA aneurysms that remain morphologically stable beyond the typical window for spontaneous regression. This case demonstrates a rare delayed thrombosis pattern after prolonged stability in a nondissecting saccular ASA aneurysm. Repeat angiographic evaluation is essential when intervention is delayed, as aneurysm status may change unexpectedly. Continued imaging surveillance remains warranted to confirm durability.

https://thejns.org/doi/10.3171/CASE26474

Isolated anterior spinal artery (ASA) aneurysms are rare vascular lesions that account for only a small fraction of spinal vascular pathologies.^1–5 Reported cases have demonstrated heterogeneous morphologies and clinical behaviors, with many lesions presumed to be dissecting in origin and frequently exhibiting fusiform configurations.^2,3,6 Owing to their rarity, the natural history of these aneurysms remains incompletely understood, and optimal management strategies have not been well established.^1,2,5,6

Spontaneous regression has been described in a substantial proportion of conservatively managed spinal artery aneurysms, particularly in small fusiform or presumed dissecting lesions.^6,7 In most reports, thrombosis or regression occurs early, within days to a few months after diagnosis.^5–7 Conversely, delayed thrombosis following prolonged morphological stability has not been well documented.

We report a ruptured ASA aneurysm that remained morphologically unchanged for nearly 1 year before undergoing complete thrombosis. Importantly, this case demonstrates delayed thrombosis after prolonged stability in a nondissecting saccular ASA aneurysm, thereby expanding the recognized temporal spectrum of aneurysm evolution. This observation also underscores the importance of repeated vascular evaluation prior to delayed intervention.

Illustrative Case

A 75-year-old man with a history of chronic hypertension presented with sudden loss of consciousness. On admission, he was in poor neurological condition (Glasgow Coma Scale score 5 [E1V1M3]). CT revealed a diffuse subarachnoid hemorrhage (Fig. 1A and B). Subsequent cerebral angiography demonstrated no intracranial aneurysm or vascular abnormality; however, a 3-mm saccular aneurysm arising from the ASA was identified at the C3 level (Fig. 1C and D).

FIG. 1.

Initial head CT scans and angiograms. A and B: CT scans demonstrating diffuse subarachnoid hemorrhage predominantly in the posterior cranial fossa. C and D:Left vertebral artery angiograms (anteroposterior projection) showing a 3-mm saccular aneurysm arising from the ASA at the C3 level (arrows).

No associated vascular abnormalities were detected, including vertebral artery stenosis, spinal arteriovenous shunt, or aortic coarctation. There were no findings suggestive of systemic connective tissue disease. The aneurysm arose focally from a normal-caliber ASA and demonstrated a well-defined neck and saccular configuration. No angiographic features suggestive of dissection, such as segmental dilatation, tapering stenosis, or vessel wall irregularity, were observed.

Because of the patient’s critical neurological status at presentation, immediate surgical or endovascular intervention was considered high risk, and conservative management was selected. Surgical exposure of a ventrally located C3 ASA aneurysm was considered technically challenging, whereas endovascular treatment carried a potential risk of parent artery compromise and spinal cord ischemia. Given the patient’s poor neurological condition, the anticipated procedural risks were considered to outweigh the uncertain risk of rebleeding. The patient therefore underwent close clinical observation during rehabilitation.

The patient received supportive care and rehabilitation, with gradual neurological improvement. During this period, management was focused on recovery from subarachnoid hemorrhage and neurological stabilization rather than definitive aneurysm treatment. No interval vascular imaging of the aneurysm was performed during rehabilitation. Over 11 months, he achieved substantial functional recovery and regained independence in daily activities.

After neurological and functional recovery had been achieved, definitive treatment of the aneurysm was reconsidered. Because the lesion remained untreated and its future rupture risk was uncertain, elective endovascular coil embolization was planned. As part of the preprocedural evaluation, repeat spinal angiography with selective microcatheterization of the ASA was performed under systemic heparinization (initial intravenous bolus 3000 U, activated clotting time maintained > 250 seconds). The aneurysm remained morphologically unchanged, with no interval growth, configuration change, or partial thrombosis, and no flow disturbance was observed (Fig. 2).

FIG. 2.

Follow-up angiograms obtained 11 months later. A: CT angiogram demonstrating a persistent 3-mm aneurysm without interval morphological change (arrow). B: Selective microcatheter angiogram of the ASA showing unchanged aneurysmal opacification with preserved patency and normal morphology of the parent ASA. C: Three-dimensional reconstruction obtained during microcatheter angiography confirming stable saccular morphology.

Four weeks later, endovascular treatment was performed under general anesthesia. However, left vertebral artery angiography ­demonstrated complete absence of aneurysmal filling. Retrograde opacification of the ASA extended to the level of the prior lesion, and right vertebral angiography demonstrated antegrade opacification up to the same level (Fig. 3), indicating preserved parent artery continuity. Therefore, selective ASA catheterization and coil embolization were not performed. MRI demonstrated isointensity on T1-weighted images and heterogeneous high to isointense signal on T2-weighted images without a flow void (Fig. 4), supporting thrombosis within the aneurysm sac. The postoperative course was uneventful. One month later, contrast-enhanced CT confirmed the persistent absence of ­aneurysmal enhancement. At the 12-month follow-up, the patient remained neurologically stable without evidence of aneurysm recanalization. Given the uncertain long-term durability of spontaneous thrombosis in spinal artery aneurysms, continued clinical and radiographic surveillance was recommended. Periodic vascular imaging was planned to monitor for possible recanalization or aneurysm recurrence.

FIG. 3.

Angiograms obtained at the time of planned endovascular treatment. A: Left vertebral artery angiogram showing complete absence of aneurysmal opacification (arrow). B: Right vertebral artery angiogram demonstrating retrograde opacification of the ASA to the level of the prior lesion (arrow), indicating preserved continuity of the parent artery.

FIG. 4.

MRI findings after aneurysm thrombosis. A: T1-weighted image showing isointensity. B: T2-weighted image demonstrating heterogeneous high to isointense signal without flow void, consistent with aneurysm sac thrombosis.

Informed Consent

The necessary informed consent was obtained in this study.

Discussion

Observations

Spontaneous regression of spinal artery aneurysms has been reported, particularly in small fusiform or presumed dissecting lesions, and typically occurs early after diagnosis.^2,3,5–7 In contrast, delayed thrombosis after prolonged morphological stability is rarely described. In the present case, the aneurysm remained morphologically unchanged over an 11-month interval without interval growth, regression, or partial thrombosis. This prolonged stability, extending well beyond the typical window for spontaneous regression, suggests that early natural involution was unlikely. The subsequent complete thrombosis observed 4 weeks later therefore represents an unusual temporal pattern and broadens the recognized spectrum of aneurysm evolution.

Evidence Supporting Isolated Aneurysm Sac Thrombosis

Several imaging findings support the interpretation of isolated aneurysm sac thrombosis rather than parent artery occlusion or dissecting pathology. Repeat angiography demonstrated complete absence of aneurysmal filling while preserving both antegrade and retrograde continuity of the ASA across the level of the prior lesion. These findings strongly argue against parent artery occlusion. Furthermore, the aneurysm arose focally from a normal-caliber ASA without angiographic features suggestive of dissection, including segmental dilatation, tapering stenosis, or vessel wall irregularity. MRI findings were also consistent with thrombosis within the aneurysm sac. Collectively, these observations support the diagnosis of isolated aneurysm sac thrombosis.

Temporal Association With Selective Angiography

The chronological sequence observed in this case—prolonged morphological stability followed by thrombosis within 4 weeks after selective angiography—is notable. A recent report of early thrombosis after microcatheter manipulation supports the idea that endovascular instrumentation can influence aneurysm biology even without embolic material.⁸ Several hypothetical mechanisms may explain such an association. Selective contrast injection into the small-caliber ASA may have transiently altered local hemodynamics and promoted intra-aneurysmal stasis. In addition, partial luminal occupation by the microcatheter itself could have temporarily reduced flow within the parent artery, resulting in decreased aneurysmal inflow and conditions favorable for thrombus formation. Although these effects would be expected to be transient, even brief flow perturbations in a low-flow spinal arterial system may initiate biological processes that culminate in delayed thrombosis. However, these mechanisms remain speculative, and a causal relationship cannot be established from a single observation. Alternative explanations, including delayed spontaneous thrombosis or subclinical vessel wall changes, remain plausible. This observation should therefore be interpreted as a temporal association rather than evidence of procedure-related causation.

Clinical Implications

This case has several practical implications. First, delayed thrombosis may occur even in ruptured ASA aneurysms that remain morphologically stable over extended periods. Second, aneurysm status may change unexpectedly, even after apparent long-term stability. Third, repeat angiographic evaluation immediately prior to delayed intervention is essential to guide appropriate management. Importantly, angiographic disappearance should not be equated with definitive cure, as recanalization and rebleeding have been described.^9,10 Continued longitudinal imaging surveillance is therefore warranted.

Lessons

Delayed thrombosis may occur in ruptured ASA aneurysms even after prolonged morphological stability. This case highlights a rare pattern of delayed thrombosis in a nondissecting saccular lesion and underscores the importance of repeat vascular evaluation prior to delayed intervention. Although a temporal association with prior angiography was observed, causality cannot be established, and continued longitudinal imaging follow-up remains necessary.

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: Maeda, Nabika, Hayashi, Mitsuhara, Ohbayashi. Acquisition of data: Hayashi, Mitsuhara. Analysis and interpretation of data: Maeda, Hayashi, Mitsuhara. Drafting the article: Maeda, Nabika, Hayashi, Mitsuhara. Critically revising the article: Hayashi. Reviewed submitted version of manuscript: Hayashi. Approved the final version of the manuscript on behalf of all authors: Maeda. Statistical analysis: Hayashi. Administrative/technical/material support: Hayashi. Study supervision: Nabika, Hayashi, Horie.

Correspondence

Yugo Maeda: Miyoshi Central Hospital, Miyoshi, Hiroshima, Japan. ygmaeda3072@gmail.com.