Spinal cord infarction after stenting for symptomatic severe stenosis of the basilar artery: a case description and literature analysis

Introduction

Stent implantation angioplasty is widely recognized as an effective treatment for patients with symptomatic intracranial atherosclerotic stenosis and can significantly improve cerebral blood flow and reduce the risk of recurrent ischemic events (1-3). However, despite its clinical benefits, this procedure is associated with several periprocedural complications, including in-stent thrombosis, hemorrhage, and hyperperfusion syndrome (4). Although these complications have been extensively documented in the literature, spinal cord infarction has rarely been reported as a potential adverse outcome following stent implantation angioplasty. Given the limited existing data on spinal cord infarction as a complication of intracranial stenting, there is a significant gap in the understanding of the mechanisms, clinical features, treatment, and prognosis of this rare but severe condition. The scarcity of reported cases and the complexity of the spinal cord’s vascular anatomy highlight the need for a comprehensive review to synthesize the available evidence and provide guidance for clinical practice. We conducted a narrative review to address this deficiency by examining the potential mechanisms underlying spinal cord infarction following intracranial stenting, summarizing the clinical features and diagnostic approaches, exploring effective treatment strategies, and evaluating the prognosis of the affected patients.

To further illuminate these critical areas, we report a case of a patient who experienced limb paralysis after basilar artery stenting, which was confirmed as spinal cord infarction via cervical spine magnetic resonance imaging (MRI). This case provides valuable insights into the potential risks and complications associated with intracranial stenting procedures.

Methods

A literature search of the PubMed, Web of Science, Scopus, and China National Knowledge Infrastructure (CNKI) databases was conducted on January 10, 2025; the specific search terms are detailed in Table 1. The search encompassed a period from January 1, 2000, to December 31, 2024, and included studies published and unpublished, such as conference abstracts and preprints, in both the English and Chinese languages. The selection process was managed by two independent reviewers (J.S. and M.L.) who evaluated the eligibility of studies based on predefined criteria, and any disagreements were resolved through discussion or, if needed, consultation with a third senior reviewer (Y.Z.). Additional considerations were noted where applicable. For detailed information, please refer to Table 1.

Case presentation

A 71-year-old woman was admitted to the Cangzhou Hospital of Integrated Traditional Chinese and Western Medicine due to dizziness and unsteady lasting 10 days, that had been aggravated for 1 day. The patient had a medical history of hypertension and coronary heart disease. For hypertension, the patient had been on antihypertensive medications, specifically 5 mg of amlodipine once daily (qd) for the previous 5 years. Despite medication, the patient’s blood pressure was often poorly controlled, with readings typically ranging from 150 to 160 mmHg systolic and 90 to 100 mmHg diastolic. Regarding coronary heart disease, the patient had myocardial infarction 3 years prior and had been taking 100 mg of aspirin daily and 20 mg of atorvastatin daily as part of secondary prevention. Regarding neurological examination, the patient was conscious, articulate, and oriented, with no abnormalities in higher cortical functions. Bilateral eyeballs moved fully in all directions without nystagmus. The pupils were equal in size and round, with brisk light reflexes. The bilateral forehead wrinkles and nasolabial folds were symmetrical, and bilateral hearing was generally normal. The tongue protruded centrally without atrophy or tremor, and the pharyngeal reflex was present, with no dysarthria. Muscle strength was grade 5 in both upper limbs and grade 4 in both lower limbs, with normal muscle tone. The finger-to-nose test and heel-knee-shin test were unstable and inaccurate. The right-sided Babinski sign was positive. Sensation, including pain, touch, temperature, position, and vibration, was normal in all four limbs, and there were no sensory deficits. Admission laboratory tests suggested hyperlipidemia (total cholesterol 5.95 mmol/L). Other laboratory tests were normal. Magnetic resonance angiography indicated basilar artery stenosis, head MRI revealed bilateral acute infarction in the cerebellar hemispheres, and carotid computed tomography angiography (CTA) showed no significant stenosis in the extracranial segment of the vertebral artery (VA) (Figure 1). The patient was initiated on dual antiplatelet therapy with aspirin and clopidogrel, along with statin therapy for lipid management. Due to suboptimal platelet aggregation response to clopidogrel [maximal aggregation rate with adenosine diphosphate (ADP) stimulation was 67.9%], clopidogrel was changed to ticagrelor to enhance antiplatelet efficacy. The stenosis in the basilar artery was identified as the primary culprit lesion, and endovascular therapy was selected to treat the severe stenosis in the basilar artery. The aim of the procedure was to improve blood flow and the reduce the risk of further ischemic events.

Figure 1 MRI showed multiple acute cerebral infarcts in the cerebellar hemispheres, and carotid CTA showed no significant stenosis in the extracranial segment of the VA. CTA, computed tomography angiography; MRI, magnetic resonance imaging; VA, vertebral artery.

All procedures in this study were performed 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 publication of this article and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Endovascular treatment

Four weeks after the onset of symptoms, we performed endovascular treatment for this patient. Under general anesthesia, a 6-F introducer sheath was inserted into the right femoral artery. Carotid angiography showed patent blood flow and visualization of the posterior communicating artery (Figure 2A-2D). Angiography of the right VA showed 95% stenosis in the lower segment of the basilar artery (Figure 2E,2F). Angiography of the left VA showed severe stenosis of the basilar artery in a localized area. The artery of Adamkiewicz (radicular artery) originated near the C2 segment on the same side, and the anterior spinal artery (ASA) was not clearly visualized (Figure 2G,2H). Subsequently, 3,000 units of heparin were administered intravenously to maintain anticoagulation, after which 1,000 units of heparin were administered intravenously every hour. Under fluoroscopic guidance, a 6-F guide catheter was advanced to the distal V2 segment of the left VA. Angiography revealed that the guide catheter was wedged and showed severe proximal stenosis of the basilar artery (Figure 3A). Repeated angiography indicated severe stenosis of the basilar artery, contrast reflux into the right VA, and a radiculomedullary artery (RMA) near the C2 level (red arrows in Figure 3B). A 300 cm, 0.014” Synchro microguidewire (Stryker, Portage, MI, USA) was delivered to the distal basilar artery (Figure 3C). A 2.0 mm × 9 mm Gateway angioplasty balloon was used to dilate the stenotic lesion, which was followed by the implantation of a 4 mm × 16 mm Enterprise self-expanding stent (Codman Neurovascular, Raynham, MA, USA). The poststent implantation angiogram revealed local thrombus formation at the junction of the vertebral and basilar arteries, near the proximal end of the implanted stent (yellow arrow in Figure 3D). Tirofiban (5 mL) was immediately administered intravenously. Repeated angiography revealed that the thrombus had migrated forward, resulting in the occlusion of the basilar artery (yellow arrow in Figure 3E). Tirofiban (5 mL) was again administered. Repeated angiography revealed that the thrombus had migrated to the distal end of the stent, with reperfusion of the distal basilar artery (yellow arrow in Figure 3F). Considering the poor response of the thrombus to tirofiban, we then mechanically disrupted the thrombus using a microguidewire and microcatheter. The final angiogram showed a patent basilar artery with no thrombosis with poor staining of the right posterior cerebral artery (blue arrows in Figure 3G). After the guide catheter was withdrawn, angiography revealed that the blood flow in the vertebral and basilar arteries was still patent, and the radicular artery at the level of C2 had the same appearance as that on preoperative imaging (Figure 3H). During the surgery, blood pressure was measured every 10 minutes. The lowest blood pressure was 115/53 mmHg, and the highest blood pressure was 128/70 mmHg. The duration of the surgery was 3 hours, with the total procedural time being 112 minutes. The guide catheter remained in the VA for 78 minutes.

Figure 2 Angiographic findings. (A-D) Carotid angiogram showed patent blood flow and visualization of the posterior communicating artery. (E,F) Angiography of the right VA showed severe stenosis of the basilar artery, with retrograde opacification of the left VA. (G,H) Angiography of the left VA showed severe stenosis of the basilar artery in a localized area. The artery of Adamkiewicz (radicular artery) originated near the C2 segment on the same side, and the ASA was not clearly visualized. ASA, anterior spinal artery; VA, vertebral artery.

Figure 3 Angiographic and procedural findings. (A) Angiography showed the presence of contrast retention and wedge of the catheter. (B) Repeat angiography showed severe stenosis of the basilar artery, with contrast reflux into the right VA and staining of the RMA near the C2 level (red arrows). (C) A 300 cm, 0.014” Synchro microguidewire was delivered to the distal basilar artery. (D) Angiography showed thrombosis after stent release (yellow arrow). (E) Angiography after the first intra-arterial administration of tirofiban showed forward movement of the thrombus (yellow arrow) and no visualization of the distal basilar artery. (F) Angiography after a second intra-arterial administration of tirofiban showed revascularization and thrombus escape to the distal end of the stent (yellow arrow). (G) The final angiogram showed a patent basilar artery with no thrombosis, with poor staining of right posterior cerebral artery (blue arrows). (H) Ten minutes after stent implantation, the blood flow within the stent was patent. RMA, radiculomedullary artery; VA, vertebral artery.

Postoperative course

The patient complained of posterior neck pain after stent implantation. On physical examination, it was found that there was a decrease in bilateral limb muscle strength (manual muscle testing score: left side limb 1/5, indicating severe weakness; right side limb 4/5, indicating mild weakness). Additionally, there was decreased pain sensation in both limbs. Given that the symptoms did not match cerebellar infarction, cervical MRI was performed. The MRI T2-weighted sequence showed high signal intensity in the spinal cord from the C2 to C4 vertebrae (Figure 4).

Figure 4 After stent implantation, the MRI T2-weighted sequence showed high signal intensity in the spinal cord from the C2 to C4 vertebrae (blue and yellow arrows). MRI, magnetic resonance imaging.

Given the clinical manifestations and radiological abnormalities, we speculated that the patient had ASA syndrome caused by spinal cord infarction. The following MRI findings suggested spinal cord infarction: (I) the T2 hyperintensity from the C2 to C4 vertebrae indicates acute ischemic injury in a vascular distribution (e.g., in the territory of the ASA). (II) The bilateral pattern and longitudinal extent aligned with the anterior spinal cord’s blood supply. (III) The acute onset following the endovascular procedure, with a plausible mechanism (catheter-related hypoperfusion or thromboembolism), matched the imaging timeline and characteristics. (IV) The lack of features such as mass effect, hemorrhage, or diffuse enhancement ruled out other possible diagnoses. The American Spinal Injury Association Impairment Scale (ASIA) was grade C. Although cerebrospinal fluid (CSF) analysis was not conducted in this case due to the strong clinical and imaging evidence, along with procedural context, supporting spinal cord infarction, we recognize that it could provide additional diagnostic clarity in distinguishing infarction from conditions such as transverse myelitis or infectious myelopathy. For such conditions, analysis of CSF might reveal pleocytosis or elevated protein levels, which are typically absent in pure ischemic injury. Future studies or cases with less clear etiologies may benefit from the use CSF examination to strengthen the differential diagnosis.

The treatment regimen was adjusted to methylprednisolone (80 mg qd) and edaravone [30 mg twice daily (bid)]. Hyperbaric oxygen therapy and rehabilitation were administered within 48 hours of the operation. Hyperbaric oxygen therapy involves air chamber, in which the patient wears a specially designed oxygen mask that receives pure oxygen. After the patient enters the chamber, the pressure inside the hyperbaric oxygen chamber gradually increases to 2 standard atmospheres over 20 minutes, is maintained for 1 hour, and then decreases to normal pressure over the next 20 minutes. The treatment course lasted for a total of 4 weeks, with 2 sessions per day in the first week and 1 session per day in the following 3 weeks. Methylprednisolone was initiated approximately 48 hours after surgery, administered as an intravenous infusion at a dose of 80 mg qd for 6 days. This was followed by 40 mg qd intravenous infusion for another 6 days. Subsequently, the patient was switched to oral administration at a dose of 20 mg qd for 3 days and then 12 mg qd for 3 days. Finally, the dose was reduced to 8 mg qd orally for 3 days before discontinuation. After treatment, the patient’s limb weakness and sensory disturbances gradually improved. On the 25th postoperative day, the patient was able to walk unassisted, with a modified Rankin Scale (mRS) score of 2, indicating mild disability. The ASIA score was grade D at hospital discharge. At the 3-month follow-up, the patient was able to perform activities of daily living independently, and her right limb pain and sensory disturbances had improved, with an mRS score of 1, indicating no significant disability. The ASIA score was grade D at 3-month follow-up.

Discussion

Due to the abundance of blood supply, spinal cord infarction is rare, accounting for 0.3–1% of all strokes (5,6). The causes of spinal cord infarction include atherosclerosis, systemic hypotension, infection, embolism, vasculitis, aortic coarctation, coagulation disorders, and medical factors, among others (7). Spinal cord infarction secondary to endovascular treatment is rare. Only six case reports, involving a total of seven patients, have described spinal cord infarction after endovascular treatment. These cases are summarized in Table 2 (8-13) and indicate that spinal cord infarction is a rare but serious complication of VA-based neurointerventions, often linked to catheter-induced flow disruption or thrombosis. Anterior cervical involvement, postoperative onset, and the need for rehabilitation are common features of these cases. The distinctive elements of each case were carefully identified and analyzed. Variations in underlying pathology, intervention complexity, spinal cord infarction, and management strategies reflect the heterogeneity of spinal cord infarction triggers and outcomes. Cases with aggressive multimodal treatment (case 1) or simpler deficits (case 5) fared better, while extensive bilateral damage (cases 2 and 6) led to poorer prognosis. This analysis underscores the need for tailored procedural precautions (catheter size and duration) and early diagnostic tools (diffusion-weighted imaging) to mitigate and detect spinal cord infarction, aligning with gaps noted in broader literature reviews on the topic (14). To the best of our knowledge, this is the first case report of spinal cord infarction following the stenting of symptomatic intracranial atherosclerosis with severe stenosis. The blood supply of the spinal cord can be divided into two parts: central and peripheral. The central part is nourished by the ASA. The peripheral part is nourished by branches of the cortical arterial plexus (coronary vessels) that surround the surface of the spinal cord, as well as branches of the ASA and posterior spinal arteries (PSAs) (7,15). In addition, some of the radicular arteries supply the dura mater, and nerve roots anastomose with the ASA or PSA and also supply the spinal cord as the RMA.

Due to anatomical variations, the blood supply to the anterior part of the upper spinal cord may primarily originate from the RMA that arises from the VA. When hemodynamic insufficiency leads to inadequate perfusion of the RMA, there may be insufficient perfusion of the corresponding segments of the ASA, leading to anterior spinal ischemia (9). Guide catheters inserted into the posterior circulation may cause the RMA of the ipsilateral VA to become hypoperfused or even thrombosed due to catheter impaction or stagnant blood flow. In four cases reviewed, catheter wedging and blood flow stasis occurred. In one case, although catheter wedging or blood flow stasis did not occur, the authors concluded that the implantation of the guide catheter still caused hypoperfusion of the ASA, leading to spinal cord infarction (16). Therefore, in patients with thinner VA diameters, a thinner guide catheter may reduce the risk of postoperative spinal cord infarction. In addition, long operation times may exacerbate hypoperfusion injury and increase the risk of thrombosis. Matsubara et al. concluded that shortening the operation time reduces the risk of spinal cord infarction after neurointerventional procedures (9). The catheter insertion time into the VA in our patient was 100 minutes, which is relatively long. This was due to the need to conduct intraoperative in-stent thrombosis and may explain why spinal cord infarction developed in the postoperative period.

Symptoms of spinal cord infarction depend on the location and extent of the infarction. Iatrogenic spinal cord infarction most commonly occurs in the cervical and thoracic medullas (17). Infarction in the area supplied by the ASA may be characterized by motor deficits in the ipsilateral limb below the plane of the diseased side. Additionally, superficial sensory deficits may occur in the contralateral limb. Sphincter dysfunction is also common. When the infarction is located in the high cervical region, respiratory failure and deep sensory deficit may occur. In addition, 59% of the patients with spinal cord infarction present with sudden onset of neck or back pain, usually radicular pain along the distribution of the affected RMA of the medulla oblongata (7,18). The onset of symptoms in the seven previously reported patients ranged from the immediate postoperative period to several days, but most occurred within 24 hours. All patients presented with limb dyskinesia and superficial sensory deficits. One exception was a case of PSA infarction, who had deep sensory deficits and poor distance discrimination. In addition, three patients had bilateral spinal cord infarcts. One of these patients had urinary deficits, and another had respiratory failure. Our patient experienced neck pain, bilateral limb weakness, bilateral superficial sensory deficits, and diaphoresis. These symptoms were not associated with respiratory failure and were noticed immediately after the operation. MRI revealed abnormal signals in the spinal cord bilaterally, which were consistent with ASA syndrome. The patient’s symptoms gradually improved within 48 hours after endovascular treatment.

Current general treatment for spinal cord infarction includes airway management, hemodynamic and fluid optimization, fever and glycemic control, anticoagulation, antiplatelet therapy, and thromboprophylaxis (19). Since the patient was found to have a spinal cord infarction for more than 24 hours, thrombolysis with alteplase was not administered. Considering the patient’s stent implantation and the possibility that the intraoperative spinal cord hypoperfusion was associated with thrombosis, we administered dual antiplatelet therapy (aspirin 100 mg qd and ticagrelor 90 mg bid). Moreover, no drugs have been developed that have a proven neuroprotective effect against spinal cord infarction in humans (19). In a prospective study, Hnath et al. found that immediate CSF drainage was effective for treating spinal cord infarction after thoracic endovascular aneurysm repair (20). However, their study did not include patients with cervical cord infarction, and thus the efficacy and safety of this treatment for cervical spinal cord infarctions after neurovascular interventions remain unclear. Therefore, we did not adopt this approach.

Ploumis et al. found that hypotension after acute spinal cord infarction can reduce spinal cord perfusion and lead to further injury due to prolonged ischemia. They recommend avoiding hypotension in the early stages and maintaining a mean arterial pressure (MAP) above 85–90 mmHg to prevent further damage (21). In our case, we maintained the patients’ MAP above 90 mmHg postoperatively. Although the efficacy of steroids in acute spinal cord injury has not been fully established (19), we administered methylprednisolone (80 mg daily) due to its anti-inflammatory and antiexudative effects.

Hyperbaric oxygen therapy increases tissue oxygenation and improves metabolism in ischemic penumbra tissue (19). Naik et al. conducted a meta-analysis and found that among patients with iatrogenic spinal cord infarction, one out of eight of those treated with hyperbaric oxygen therapy showed improvement, with six achieving almost complete recovery (22). Our patient was subjected to hyperbaric oxygen therapy immediately upon diagnosis of spinal cord infarction. For the first 7 days, the therapy was administered bid, and then it was adjusted to once a day. Interestingly, we observed a significant difference in our patients’ condition before and after a single session of hyperbaric oxygen therapy, which suggests its potential efficacy in clinical management. Lee et al. reported a case of spinal cord infarction in which the combination of recombinant tissue plasminogen activator (rtPA) arteriovenous thrombolysis, hyperbaric oxygen therapy, and subcooling therapy significantly alleviated the patient’s symptoms. However, it was unclear which specific measure was decisive. The authors suggested that a multimodal approach, including intravenous and arterial thrombolysis, hyperbaric oxygen therapy, and hypothermia, is feasible treatment strategy for spinal cord infarction (8). Other therapeutic measures mentioned were primarily related to rehabilitation (Table 2).

The prognosis for spinal cord infarction is generally poor, with an acute mortality rate of approximately 20%, and severe neurological sequelae observed in over 50% of affected patients (5). A recently published literature review indicates that after spinal cord infarction, neurological recovery is to be expected, with the majority of patients regaining ambulation (23). A study of 22 patients with spinal infarction for an average of 18 months found that 55% had an unfavorable outcome (22). Romi et al. found that compared with patients with cerebral infarction, patients with spinal infarction may have a better outcome after initial treatment but are more likely to experience long-term chronic pain (24). In this study, none of the eight patients had long-term follow-up outcomes. Specifically, two cases failed to report the follow-up duration and patient status (9); among the remaining six patients, two had an mRS score of 4, indicating an unfavorable outcome. The possible reason for the poor prognosis was severe initial injury (respiratory failure occurred) or a late diagnosis of postoperative cervical infarction (7 days after symptoms appeared). Of the remaining four patients, two had an mRS score of 2 and two had an mRS score of 1. The two patients with a follow-up mRS score of 1 both received hyperbaric oxygen therapy during treatment. Overall, patients with severe initial injury from spinal cord infarction may have a poor prognosis.

CSF analysis was not conducted in our case due to the strong clinical and imaging evidence, along with the procedural context, supporting a diagnosis of spinal cord infarction. However, we recognize that CSF analysis could provide additional diagnostic clarity in distinguishing infarction from conditions such as transverse myelitis or infectious myelopathy. For these conditions, CSF might reveal pleocytosis or elevated protein levels, which are typically absent in pure ischemic injury. Despite not being performed in our case, CSF examination could be considered in other cases to rule out inflammatory or infectious mimics more definitively, particularly when the clinical presentation or imaging findings are less conclusive. Further studies incorporating CSF data could strengthen the diagnostic framework for this rare complication.

Conclusions

We report a case of spinal cord infarction after basilar artery stent implantation. Using thinner guide catheters and reducing procedure time may help prevent spinal cord infarction in patients with thin VAs after endovascular therapy. Hyperbaric oxygen therapy may be an effective treatment.

Acknowledgments

None.

Footnote

Funding: This study was supported by by Cangzhou Key Research and Development Program Project (to J.S.) (No. 213106137).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-332/coif). The 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 Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for publication of this article 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. Chimowitz MI, Lynn MJ, Derdeyn CP, Turan TN, Fiorella D, Lane BF, et al. Stenting versus aggressive medical therapy for intracranial arterial stenosis. N Engl J Med 2011;365:993-1003. Erratum in: N Engl J Med 2012;367:93. [Crossref] [PubMed]
2. Miao Z, Zhang Y, Shuai J, Jiang C, Zhu Q, Chen K, Liu L, Li B, Shi X, Gao L, Liu Y, Wang F, Li Y, Liu T, Zheng H, Wang Y, Wang YStudy Group of Registry Study of Stenting for Symptomatic Intracranial Artery Stenosis in China. Thirty-Day Outcome of a Multicenter Registry Study of Stenting for Symptomatic Intracranial Artery Stenosis in China. Stroke 2015;46:2822-9. [Crossref] [PubMed]
3. Huang K, Yao W, Zha M, Qin S, Li Y, Xu Y, Liu R, Ye R, Han Y, Zhu W, Teng Z, Du J, Liu X. Angiography-based hemodynamic features predict recurrent ischemic events after angioplasty and stenting of intracranial vertebrobasilar atherosclerotic stenosis. Eur Radiol 2024;34:2352-63. [Crossref] [PubMed]
4. Riedel CH, Tietke M, Alfke K, Stingele R, Jansen O. Subacute stent thrombosis in intracranial stenting. Stroke 2009;40:1310-4. [Crossref] [PubMed]
5. Leys D, Pruvo JP. Spinal infarcts. Rev Neurol (Paris) 2021;177:459-68. [Crossref] [PubMed]
6. Hanna Al-Shaikh R, Czervionke L, Eidelman B, Dredla BK. Spinal Cord Infarction. In: StatPearls. Treasure Island: StatPearls Publishing; 2023.
7. Vuong SM, Jeong WJ, Morales H, Abruzzo TA. Vascular Diseases of the Spinal Cord: Infarction, Hemorrhage, and Venous Congestive Myelopathy. Semin Ultrasound CT MR 2016;37:466-81. [Crossref] [PubMed]
8. Lee K, Strozyk D, Rahman C, Lee LK, Fernandes EM, Claassen J, Badjatia N, Mayer SA, Pile-Spellman J. Acute spinal cord ischemia: treatment with intravenous and intra-arterial thrombolysis, hyperbaric oxygen and hypothermia. Cerebrovasc Dis 2010;29:95-8. [Crossref] [PubMed]
9. Matsubara N, Miyachi S, Okamaoto T, Izumi T, Asai T, Yamanouchi T, Ota K, Oda K, Wakabayashi T. Spinal cord infarction is an unusual complication of intracranial neuroendovascular intervention. Interv Neuroradiol 2013;19:500-5. [Crossref] [PubMed]
10. Iwahashi H, Fujita A, Tanaka H, Ikeda M, Morikawa M, Kohmura E. Spinal cord infarction after successful coil embolization of recurrent basilar bifurcation aneurysm: a case report. J Neuroendovasc Ther 2018;12:398-403.
11. Elzamly K, Nobleza C, Parker E, Sugg R. Unilateral Upper Cervical Posterior Spinal Cord Infarction after a Neuroendovascular Intervention: A Case Report. Case Rep Neurol Med 2018;2018:5070712. [Crossref] [PubMed]
12. Masson C, Pruvo JP, Meder JF, Cordonnier C, Touzé E, De La Sayette V, Giroud M, Mas JL, Leys DStudy Group on Spinal Cord Infarction of the French Neurovascular Society. Spinal cord infarction: clinical and magnetic resonance imaging findings and short term outcome. J Neurol Neurosurg Psychiatry 2004;75:1431-5. [Crossref] [PubMed]
13. Imura J, Fujita A, Umeda S, Fujimoto Y, Kohta M, Sasayama T. Spinal cord infarction after coil embolization of a basilar tip aneurysm: A case report and literature review. Surg Neurol Int 2022;13:415. [Crossref] [PubMed]
14. Chen H, Xu Z, Fu Y. Spinal cord infarction following neurointerventional procedures in the posterior cerebral circulation: a case analysis and systematic literature review. BMC Neurol 2025;25:232. [Crossref] [PubMed]
15. Martirosyan NL, Feuerstein JS, Theodore N, Cavalcanti DD, Spetzler RF, Preul MC. Blood supply and vascular reactivity of the spinal cord under normal and pathological conditions. J Neurosurg Spine 2011;15:238-51. [Crossref] [PubMed]
16. Moazeni Y, Cantrell DR, Clark JR, Abdalla RN, Batra A, Hurley MC, Ansari SA, Russell EJ, Shaibani A. Case Report: Anterior Spinal Cord Ischemia Following Embolization of Cerebellar Arteriovenous Malformation: An Illustrative Case and Review of Spinal Cord Vascular Anatomy. Front Neurol 2021;12:725065. [Crossref] [PubMed]
17. Montalva-Iborra A, Alcanyis-Alberola M, Grao-Castellote C, Torralba-Collados F, Giner-Pascual M. Risk factors in iatrogenic spinal cord injury. Spinal Cord 2017;55:818-22. [Crossref] [PubMed]
18. Nasr DM, Rabinstein A. Spinal Cord Infarcts: Risk Factors, Management, and Prognosis. Curr Treat Options Neurol 2017;19:28. [Crossref] [PubMed]
19. Nardone R, Pikija S, Mutzenbach JS, Seidl M, Leis S, Trinka E, Sellner J. Current and emerging treatment options for spinal cord ischemia. Drug Discov Today 2016;21:1632-41. [Crossref] [PubMed]
20. Hnath JC, Mehta M, Taggert JB, Sternbach Y, Roddy SP, Kreienberg PB, Ozsvath KJ, Chang BB, Shah DM, Darling RC 3rd. Strategies to improve spinal cord ischemia in endovascular thoracic aortic repair: Outcomes of a prospective cerebrospinal fluid drainage protocol. J Vasc Surg 2008;48:836-40. [Crossref] [PubMed]
21. Ploumis A, Yadlapalli N, Fehlings MG, Kwon BK, Vaccaro AR. A systematic review of the evidence supporting a role for vasopressor support in acute SCI. Spinal Cord 2010;48:356-62. [Crossref] [PubMed]
22. Naik A, Moawad CM, Houser SL, Kesavadas TK, Arnold PM. Iatrogenic spinal cord ischemia: A patient level meta-analysis of 74 case reports and series. N Am Spine Soc J 2021;8:100080. [Crossref] [PubMed]
23. Gharios M, Stenimahitis V, El-Hajj VG, Mahdi OA, Fletcher-Sandersjöö A, Jabbour P, Andersson M, Hultling C, Elmi-Terander A, Edström E. Spontaneous spinal cord infarction: a systematic review. BMJ Neurol Open 2024;6:e000754. [Crossref] [PubMed]
24. Romi F, Naess H. Spinal Cord Infarction in Clinical Neurology: A Review of Characteristics and Long-Term Prognosis in Comparison to Cerebral Infarction. Eur Neurol 2016;76:95-8. [Crossref] [PubMed]