A Truman show in acute ischemic stroke: live demonstration of the journey from large vessel stenosis to occlusion in minor stroke

Introduction

Background

Acute ischemic stroke (AIS), caused by sudden interruption of cerebral blood flow due to arterial occlusion, accounts for approximately 80–85% of all stroke cases. The risk increases with age and is strongly associated with vascular risk factors such as hypertension, diabetes mellitus, hyperlipidemia, smoking, and atrial fibrillation. Patients typically present with sudden focal neurological deficits, including unilateral weakness, speech disturbances, visual changes, or imbalance (1,2). Timely reperfusion is critical to minimize brain injury. Current treatments include intravenous thrombolysis within 4.5 hours and endovascular thrombectomy for eligible large vessel occlusions (LVOs), alongside long-term secondary prevention (3,4).

Abrupt hemodynamic shifts may unmask critical stenoses in patients with intracranial atherosclerotic disease (ICAD). The relationship between vasomotor tone, blood pressure fluctuations, and vessel patency is increasingly recognized (5) but seldom directly demonstrated angiographically. Here we report a case of AIS where an initially patent, severe ICAD lesion abruptly progressed to complete occlusion following general anesthesia (GA)-induced hypotension. This case is unique in providing real-time angiographic evidence of hemodynamic instability directly precipitating LVO, contributing to a better understanding of dynamic lesion behavior and guiding risk stratification in ICAD management.

Rationale and knowledge gap

Although the hemodynamic instability of intracranial atherosclerotic stenotic (ICAS) lesions is recognized, real-time angiographic documentation of stenotic lesions acutely progressing to occlusion remains rare. Fluctuations in blood pressure, vasomotor tone, or systemic factors (e.g., sleep, anesthesia, or exertion) may precipitate sudden occlusion in critically narrowed vessels. However, such events are often inferred clinically rather than directly observed. There is limited guidance on identifying high-risk ICAS lesions at risk of such abrupt progression and on optimal timing for intervention.

Objective

We present a case of acute mild ischemic stroke in which a severe ICAS lesion progressed to an on-table M1 middle cerebral artery (MCA) LVO following GA-induced hypotension. This case provides real-time angiographic evidence of dynamic lesion behavior under hemodynamic stress and highlights the potential benefit of early endovascular thrombectomy (EVT) in selected high-risk patients with severe intracranial stenosis (>70%), fluctuating or progressive neurological symptoms, impaired collateral circulation, hemodynamic dependence, or recurrent ischemic events despite medical therapy, who may be particularly vulnerable to abrupt occlusion under conditions of blood pressure fluctuation or vasomotor instability. We present this article in accordance with the CARE reporting checklist (available at https://jni.amegroups.com/article/view/10.21037/jni-25-6/rc).

Case presentation

A patient in his 70s presented with expressive dysphasia, right facial droop, left gaze deviation, and right upper limb weakness with impaired dexterity for 3–4 hours. On admission, his blood pressure was 160/90 mmHg, and the National Institutes of Health Stroke Scale (NIHSS) score was 4. His medical history included chronic smoking, hypertension, and hyperlipidemia. He was taking amlodipine 10 mg once daily and atorvastatin 40 mg once daily. Admission blood sugar level was 11.0 mmol/L, consistent with hyperglycemia.

Non-contrast computed tomography (CT) of the brain showed no intracranial hemorrhage or large infarct core [Alberta Stroke Program Early CT Score (ASPECTS) 10]. CT angiography demonstrated a focal occlusion in the left M1 segment of the MCA. An emergency diagnostic cerebral angiogram was performed under local anesthesia to further characterize the lesion. Angiography revealed severe focal stenosis in the mid-M1 MCA and a tandem stenotic lesion at the MCA bifurcation, with sluggish antegrade flow (Figure 1). Following multidisciplinary discussion, a consensus decision was made to proceed with primary intracranial angioplasty for this hemodynamically significant focal ICAS lesion.

Figure 1 Left MCA ICAD lesions—severe stenosis at M1 (arrow). ICAD, intracranial atherosclerotic disease; MCA, middle cerebral artery.

The patient was placed under GA for the procedure. During induction, there was a transient drop in systolic blood pressure to just below 90 mmHg [mean arterial pressure (MAP) ~70 mmHg]. During induction, systolic blood pressure transiently dropped to just below 90 mmHg (MAP ~70 mmHg) for approximately 2–3 minutes. Intravenous vasopressors were administered to promptly restore blood pressure to baseline levels. However, the occlusion had already occurred during this brief hypotensive window which angiography demonstrated complete occlusion of the previously patent left M1 MCA (Figure 2). Delivery system assembly consisting of 6-F NeuronMAX guiding catheter (Penumbra, Alameda, CA, USA) was advanced to left internal carotid artery (ICA). The left M1 MCA occlusion was crossed with a 0.021-inch Rebar microcatheter (Medtronic, Minneapolis, MN, USA) and 0.014-inch Transend guidewire (Boston Scientific, Fremont, CA, USA) (Figure 3). A 4 mm × 20 mm Solitaire AB stent-retriever (Medtronic) was deployed from the proximal M2 into the M1 MCA, spanning the occlusion and previously seen distal M1 stenosis (Figure 4). Intravenous eptifibatide 8 mg was administered and after a 5-minute dwell time, the stent was retrieved. Follow-up angiography demonstrated excellent antegrade flow with first-pass thrombolysis in cerebral infarction (TICI) 3 reperfusion. Residual 30% stenosis remained at the mid-M1 segment with mild-to-moderate tandem residual stenosis at the distal M1. Aspirin 300 mg was administered via nasogastric tube. Repeat angiograms at 5, 10, and 25 minutes confirmed sustained patency without re-occlusion (Figure 5). The procedure was uneventfully concluded.

Figure 2 Left MCA after GA induction—completely occluded. GA, general anesthesia; MCA, middle cerebral artery.

Figure 3 Crossing left M1 MCA occlusion with Phenom 021 and contrast injection to confirm intraluminal placement. MCA, middle cerebral artery.

Figure 4 Fluoroscopic snapshots of stent-retriever deployment. (A) Deployment of the Solitaire AB 4 mm × 20 mm stent-retriever (Medtronic) across the M1 occlusion for mechanical thrombectomy. The stent spans the occluded segment and underlying stenosis. (B) Stent left deployed for 5 minutes to achieve stentoplasty effect, allowing stretching of the underlying stenotic segment while simultaneously capturing thrombus.

Figure 5 Serial left ICA DSA obtained post-thrombectomy at 5 (A) and 25 minutes (B), demonstrating sustained patency of the recanalized M1 segment without evidence of re-occlusion or distal embolization. (A) Left ICA DSA at 5 minutes post-thrombectomy showing excellent antegrade flow through the left MCA with no residual occlusion. (B) Left ICA DSA at 25 minutes post-thrombectomy confirming persistent vessel patency and stable perfusion, without interval re-occlusion or delayed thrombotic events. DSA, digital subtraction angiograms; ICA, internal carotid artery.

Dual antiplatelet therapy (DAPT) consisting of aspirin 100 mg and clopidogrel 75 mg daily was initiated the next day. The patient’s neurological deficits improved significantly. At discharge (3 days post-procedure), he was functionally independent with only mild word-finding difficulties [Montreal Cognitive Assessment (MoCA) 26/30]. The NIHSS score was 1 and modified Rankin Scale (mRS) score was 2 at discharge. The post-operative course was uneventful, and patient was well upon discharge (Table 1).

At 3-month clinical follow-up, the patient remained functionally independent (mRS 1) without recurrent neurological events or clinical deterioration. No interval imaging showed evidence of re-occlusion or new ischemic lesions.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

We report a unique case of dynamic ICAS where a previously patent, high-grade M1 MCA ICAS lesion acutely progressed to complete occlusion following GA-induced hypotension. While hemodynamic instability is a recognized risk in patients with ICAD, real-time angiographic documentation of on-table abrupt occlusion triggered by anesthesia remains rare. In most prior reports, deterioration is often observed clinically or inferred through delayed neuroimaging following sleep, exertion, or hemodynamic fluctuation, but direct intra-procedural imaging evidence remains limited (6,7). Our case demonstrates how systemic hypotension during induction of anesthesia can unmask critical stenoses and result in emergent LVO.

Strengths and limitations

A major strength of this report is the direct angiographic capture of acute ICAS instability, providing real-time insight into dynamic lesion behavior under controlled conditions. The report further demonstrates a successful technical strategy combining mechanical thrombectomy, stentoplasty effect, and adjunctive glycoprotein IIb/IIIa inhibition.

The primary limitation remains its nature as a single case report. Collateral circulation, plaque morphology, or cerebral perfusion reserve were not quantitatively assessed and may have contributed to the observed outcome. Although favorable reperfusion and clinical recovery were achieved, whether earlier intervention prior to GA induction may have prevented occlusion remains speculative. The role of glycoprotein IIb/IIIa inhibitors, including optimal dosing and timing, also remains unvalidated in this context.

Comparison with similar research

While several studies have reported worsening of minor stroke symptoms in patients with ICAD under conditions of hypotension or during sleep, direct angiographic evidence of abrupt on-table occlusion remains scarce (6-8). Our case adds to a limited body of literature by directly documenting such an event intra-procedurally. It supports prior findings suggesting that hemodynamic fluctuations can precipitate occlusion in unstable ICAS lesions and further emphasizes the need for risk stratification in this patient subgroup.

Explanations of findings

In this case, the induction of GA likely triggered cerebral autoregulatory failure, lowering distal perfusion pressure and contributing to abrupt vessel closure.8 However, we acknowledge this remains a likely but unproven mechanism. Additional contributors may include impaired collateral support, plaque instability, and platelet activation. Furthermore, posture and positioning may modulate cerebral perfusion, particularly in intensive care unit (ICU) settings or sedated patients where head or neck positioning alters intracranial hemodynamics (9,10). The technical success of stent-retriever thrombectomy with stentoplasty effect aligns with previous reports showing mechanical thrombectomy with angioplasty as an effective rescue strategy in ICAD-related LVO (11). The use of eptifibatide, a glycoprotein IIb/IIIa inhibitor, aimed to prevent platelet aggregation and minimize re-occlusion risk during and after stent-retriever dwell time (12,13). Hyperglycemia of 11 mmol/L at admission may have further exacerbated microvascular dysfunction and prothrombotic tendency, contributing to ischemic risk, as previously reported (14,15). Despite these complex contributing factors, post-discharge follow-up showed no recurrent events and stable vessel patency.

Implications and actions needed

This case highlights the need for heightened vigilance regarding anesthesia choice in patients with severe ICAD undergoing endovascular procedures. Conscious sedation may provide better hemodynamic stability, but prospective studies are required to clarify its role. Careful peri-procedural blood pressure monitoring, proactive correction of hypotension, and attention to patient positioning may help reduce risk of dynamic occlusion. Furthermore, early identification of high-risk ICAD patients—including those with severe stenosis, fluctuating symptoms, impaired collaterals, and metabolic risk factors—may help guide more proactive treatment strategies before irreversible occlusion occurs.

Conclusions

This case provides direct angiographic evidence of dynamic ICAD progression, where GA-induced hypotension likely precipitated abrupt LVO in a previously patent high-grade stenosis. The successful outcome highlights the potential benefit of timely endovascular intervention, combined stent-retriever thrombectomy with stentoplasty effect, and adjunctive antiplatelet therapy in managing unstable intracranial stenoses. Careful patient selection, hemodynamic management, and procedural planning are crucial in high-risk ICAD cases to prevent sudden deterioration. Further studies are needed to optimize treatment strategies and identify patients most likely to benefit from early intervention.

Acknowledgments

The authors would like to thank the neurointerventional, anesthesiology, and stroke neurology teams involved in the management of this case.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://jni.amegroups.com/article/view/10.21037/jni-25-6/rc

Peer Review File: Available at https://jni.amegroups.com/article/view/10.21037/jni-25-6/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jni.amegroups.com/article/view/10.21037/amj-25-6/coif). G.A. served as a consultant for Medtronic, BD, Balt, Stryker, and Penumbra. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Donnan GA, Fisher M, Macleod M, et al. Stroke. Lancet 2008;371:1612-23. [Crossref] [PubMed]
2. Feigin VL, Brainin M, Norrving B, et al. World Stroke Organization (WSO): Global Stroke Fact Sheet 2022. Int J Stroke 2022;17:18-29. [Crossref] [PubMed]
3. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2019;50:e344-418. [Crossref] [PubMed]
4. Mokin M, Jovin TG, Sheth SA, et al. Endovascular therapy in patients with acute ischemic stroke with large infarct: A guideline from the Society of vascular and Interventional Neurology. Stroke Vasc Interv Neurol 2025;5:e001581.
5. Hoh BL, Chimowitz MI. Focused Update on Intracranial Atherosclerosis: Introduction, Highlights, and Knowledge Gaps. Stroke 2024;55:305-10. [Crossref] [PubMed]
6. de Havenon A, Zaidat OO, Amin-Hanjani S, et al. Large Vessel Occlusion Stroke due to Intracranial Atherosclerotic Disease: Identification, Medical and Interventional Treatment, and Outcomes. Stroke 2023;54:1695-705. [Crossref] [PubMed]
7. Chen Z, Liu J, Wang A, et al. Hemodynamic Impairment of Blood Pressure and Stroke Mechanisms in Symptomatic Intracranial Atherosclerotic Stenosis. Stroke 2024;55:1798-807. [Crossref] [PubMed]
8. Liu Y, Li S, Tian X, et al. Cerebral haemodynamics in symptomatic intracranial atherosclerotic disease: a narrative review of the assessment methods and clinical implications. Stroke Vasc Neurol 2023;8:521-30. [Crossref] [PubMed]
9. Hifumi T, Yamakawa K, Shiba D, et al. Head positioning in suspected patients with acute stroke from prehospital to emergency department settings: a systematic review and meta-analysis. Acute Med Surg 2021;8:e631. [Crossref] [PubMed]
10. Lam MY, Haunton VJ, Nath M, et al. The effect of head positioning on cerebral hemodynamics: Experiences in mild ischemic stroke. J Neurol Sci 2020;419:117201. [Crossref] [PubMed]
11. Beaman C, Yaghi S, Liebeskind DS. A decade on: the evolving renaissance in intracranial atherosclerotic disease. Stroke Vasc Interv Neurol 2022;2:e000497.
12. Chahal H, Mehta S, Moussavi M, et al. Eptifibatide is safe and may improve outcomes in stroke patients undergoing Thrombectomy after receiving IVtPA (P2. 276). Neurology 2016;86:P2.276.
13. Ma G, Sun X, Cheng H, et al. Combined Approach to Eptifibatide and Thrombectomy in Acute Ischemic Stroke Because of Large Vessel Occlusion: A Matched-Control Analysis. Stroke 2022;53:1580-8. [Crossref] [PubMed]
14. Kim JT, Jahan R, Saver JL, et al. Impact of Glucose on Outcomes in Patients Treated With Mechanical Thrombectomy: A Post Hoc Analysis of the Solitaire Flow Restoration With the Intention for Thrombectomy Study. Stroke 2016;47:120-7. [Crossref] [PubMed]
15. Belge Bilgin G, Bilgin C, Jabal MS, et al. The effects of admission hyperglycemia and diabetes mellitus on mechanical thrombectomy outcomes: A systematic review and meta-analysis. Interv Neuroradiol 2025; Epub ahead of print. [Crossref]