Anterior Spinal Artery Syndrome

1. Disease Information

1.1 What is the disease?

ASAS is a clinical syndrome reflecting ischemic injury in the vascular territory of the anterior spinal artery, usually due to spinal cord infarction. Reviews and case reports consistently frame ASAS as ischemia/obstruction of ASA supply to the anterior two‑thirds of the spinal cord; the tract-level anatomy explains the characteristic dissociation of modalities (motor and pain/temperature more affected than dorsal column modalities). (althobaiti2024anteriorspinalartery pages 1-3, zedde2025spinalcordinfarction pages 2-4)

Direct abstract-supported definition (example, 2023 case literature): Waack et al. state: “Anterior cord syndrome (ACS) occurs as a result of ischemia in the territory of the anterior spinal artery (ASA),” and describe the typical presentation and tract correlates. https://doi.org/10.7759/cureus.40391 (published Jun 2023). (islam2021anteriorspinalartery pages 7-9)

1.2 Key identifiers (OMIM/Orphanet/ICD/MeSH/MONDO)

• MONDO / Orphanet / OMIM: In the retrieved primary literature set, formal MONDO/Orphanet/OMIM IDs were not provided, and ASAS is generally treated as a syndrome/phenotype of vascular spinal cord infarction rather than a monogenic disorder. (althobaiti2024anteriorspinalartery pages 1-3, zedde2025spinalcordinfarction pages 2-4)
• ICD coding: The retrieved corpus did not include a definitive ICD-10/ICD-11 code mapping for “anterior spinal artery syndrome” specifically; contemporary epidemiologic work tends to code at the level of “spinal cord infarction/ischemia” or related stroke/myelopathy categories rather than syndrome-specific labels. (althobaiti2024anteriorspinalartery pages 1-3)
• MeSH: The tool-retrieved content did not provide a direct MeSH descriptor ID for “anterior spinal artery syndrome.” (sliwa1992ischemicmyelopathya pages 1-2)

Knowledge-base note: For a practical knowledge base, ASAS is often represented under broader entities such as “spinal cord infarction,” with ASAS as a clinical presentation subtype. (zedde2025spinalcordinfarction pages 2-4, althobaiti2024anteriorspinalartery pages 1-3)

1.3 Common synonyms and alternative names

Synonyms used in recent literature include: * Anterior cord syndrome (explicitly: “ASAS, alternatively termed anterior cord syndrome”) (althobaiti2024anteriorspinalartery pages 6-7) * Anterior spinal cord infarction and spinal stroke as closely related clinical terms used for the same vascular entity/presentation (althobaiti2024anteriorspinalartery pages 1-3) * Related terms used in search strategies and case literature include spinal cord infarct, spinal cord ischemia, and ASA occlusion/dissection/compression language. (islam2021anteriorspinalartery pages 4-7)

1.4 Evidence source types

The ASAS evidence base is largely: * Aggregated disease-level resources: narrative reviews and systematic reviews of spinal cord infarction/ischemia and aortic surgery complications (batsou2023spinalcordischemia pages 3-3, zedde2025spinalcordinfarction pages 2-4, torre2024enhancingneuroprotectionin pages 8-10) * Human clinical observational cohorts/series (e.g., cohort distributions of SCI subtypes; post-aortic repair prevention protocols) (nagoshi2025imagingcharacteristicsclinical pages 5-8, rosvall2024adedicatedpreventive pages 1-2) * Case reports (helpful for rare iatrogenic triggers and mimics) (althobaiti2024anteriorspinalartery pages 1-3)

2. Etiology

2.1 Disease causal factors (mechanistic)

Causation is typically vascular (arterial occlusion, embolism, or hypoperfusion), leading to ischemic necrosis of the anterior spinal cord (gray matter and adjacent white matter). (zedde2025spinalcordinfarction pages 2-4, batsou2023spinalcordischemia pages 3-3)

2.2 Risk factors (human clinical)

Commonly reported etiologies/risk contexts include: * Aortic disease and aortic procedures (open thoracoabdominal aortic surgery; endovascular repair/EVAR/TEVAR) (zedde2025spinalcordinfarction pages 2-4, rosvall2024adedicatedpreventive pages 1-2) * Systemic hypotension / low-flow states (perioperative or spontaneous) (batsou2023spinalcordischemia pages 3-3, althobaiti2024anteriorspinalartery pages 6-7) * Embolic causes (cardiac embolism; fibrocartilaginous embolism in some contexts) (althobaiti2024anteriorspinalartery pages 6-7, zedde2025spinalcordinfarction pages 2-4) * Vertebral artery dissection/occlusion and posterior circulation procedures causing cervical SCI via hypoperfusion/occlusion (as a general SCI mechanism, relevant to ASA territory) (althobaiti2024anteriorspinalartery pages 6-7) * Neuraxial anesthesia/epidural procedures as iatrogenic contributors in cohort data (nagoshi2025imagingcharacteristicsclinical pages 5-8)

Quantitative vascular risk factor burden: One review summarized that “one or more vascular risk factors” were present in 76% of patients in one study, pooled “at least 1 vascular risk factor” in 81%, and “at least 3” in 45.5%. (batsou2023spinalcordischemia pages 1-2)

Procedure-associated burden: In a 19-patient Japanese cohort (2012–2022), 57.9% of SCI cases were iatrogenic (post-cardiac surgery and epidural anesthesia). (nagoshi2025imagingcharacteristicsclinical pages 5-8)

2.3 Protective factors

Specific protective genetic or environmental factors for ASAS are not well-established in the retrieved literature. In the aortic-surgery context, “protective” measures are largely procedural/perfusion optimization strategies (see Prevention/Treatment sections). (rosvall2024adedicatedpreventive pages 1-2, sufali2024resultsofa pages 1-3)

2.4 Gene–environment interactions

No robust gene–environment interaction framework specific to ASAS was identified in the retrieved papers; however, vascular risk factors (smoking, hypertension, dyslipidemia, diabetes) interact with major environmental/iatrogenic triggers (aortic interventions, hypotension) to influence risk. (zedde2025spinalcordinfarction pages 2-4, althobaiti2024anteriorspinalartery pages 6-7)

3. Phenotypes

3.1 Core phenotypes and suggested HPO terms

Typical clinical features (with suggested HPO mappings): * Acute paraparesis/paraplegia → Paraplegia (HP:0003401), Paraparesis (HP:0001258) * Acute quadriparesis (cervical lesions) → Quadriparesis (HP:0000749) * Loss of pain and temperature sensation → Impaired pain sensation (HP:0007025), Abnormality of temperature sensation (HP:0004370) * Relative sparing of vibration/proprioception (clinical dissociation; often described qualitatively) → consider annotating Normal proprioception (not standard HPO phenotype; document as “dorsal column sparing” clinical feature) * Autonomic dysfunction: urinary retention/incontinence → Urinary retention (HP:0000016) / Urinary incontinence (HP:0000020); bowel dysfunction → Constipation (HP:0002019) or Fecal incontinence (HP:0002607) * Acute back/neck pain → Back pain (HP:0003418), Neck pain (HP:0000467)

These features are repeatedly emphasized in contemporary case literature describing sudden pain and bilateral paralysis with pain/temperature loss and dorsal column sparing, plus autonomic symptoms. (althobaiti2024anteriorspinalartery pages 1-3, islam2021anteriorspinalartery pages 7-9)

3.2 Phenotype characteristics (onset, progression, frequency)

• Temporal pattern: Rapid progression to severe deficit is typical; diagnostic reviews emphasize time to nadir <12 h as a strong clinical predictor for spinal cord infarction diagnosis. (zedde2025spinalcordinfarction pages 2-4)
• Quantitative time-to-nadir distribution (meta-analysis): <6 h 56.1%, 6–12 h 30.7%, 12–72 h 5.4%, >72 h 7.8%. (batsou2023spinalcordischemia pages 3-3)
• Frequency among SCI: In one 19-case cohort, 12/19 presented with ASA syndrome. (nagoshi2025imagingcharacteristicsclinical pages 5-8)

3.3 Quality of life impact

ASAS frequently causes persistent gait impairment and autonomic dysfunction requiring prolonged rehabilitation and long-term support; functional outcomes often reflect initial severity. (batsou2023spinalcordischemia pages 3-3, nagoshi2025imagingcharacteristicsclinical pages 5-8)

4. Genetic / Molecular Information

4.1 Causal genes

ASAS is not typically a monogenic disorder; it is a vascular syndrome. No causal gene list for ASAS exists in the retrieved primary sources. (zedde2025spinalcordinfarction pages 2-4, althobaiti2024anteriorspinalartery pages 1-3)

4.2 Pathogenic variants / modifier genes

Specific inherited thrombophilias are occasionally reported in spinal cord ischemia case literature (outside the retrieved ASAS-focused core set), but within the evidence assembled here, thrombophilia and coagulopathy are treated as risk contexts rather than defining genetic causes. (althobaiti2024anteriorspinalartery pages 6-7)

4.3 Molecular pathways (inferred, not disease-specific omics)

Although ASAS lacks disease-specific omics studies in the retrieved set, ischemia-reperfusion biology implies involvement of: * excitotoxicity, oxidative stress, neuroinflammation, endothelial dysfunction, and microvascular failure. Aortic cross-clamp model review notes predominant gray matter (neuronal) injury and variable subsequent white matter injury, supporting selective anterior horn vulnerability. (awad2021histologicalfindingsafter pages 13-14)

5. Environmental Information

5.1 Environmental and lifestyle risk factors

The main “environmental” contributors are vascular risk behaviors and comorbidities (e.g., smoking, hypertension, dyslipidemia), plus iatrogenic exposures (aortic procedures, neuraxial anesthesia). A review reports smoking prevalence around 30%, hypertension 40%, dyslipidemia 29%, diabetes 16% among SCI cases in one synthesis. (zedde2025spinalcordinfarction pages 2-4)

5.2 Infectious agents

No specific infectious causal agent is established for ASAS in the retrieved evidence set. (zedde2025spinalcordinfarction pages 2-4)

6. Mechanism / Pathophysiology

6.1 Causal chain (clinical mechanism)

1. Trigger: ASA occlusion, embolus, hypoperfusion (hypotension), or peri-aortic procedure collateral disruption. (batsou2023spinalcordischemia pages 3-3, zedde2025spinalcordinfarction pages 2-4)
2. Primary lesion: ischemia of ASA territory (anterior two‑thirds), especially metabolically vulnerable gray matter/anterior horns. (zedde2025spinalcordinfarction pages 2-4, awad2021histologicalfindingsafter pages 13-14)
3. Clinical manifestation: motor deficits (corticospinal/anterior horn), pain/temperature loss (spinothalamic), autonomic dysfunction (lateral horn/intermediolateral cell columns), with dorsal column sparing. (zedde2025spinalcordinfarction pages 2-4, althobaiti2024anteriorspinalartery pages 1-3)

6.2 Tissue injury mechanisms

Preclinical aortic cross-clamp models show a conserved pattern: injury is “predominantly in the grey matter,” with anterior gray matter often worse, and white matter injury emerging later. (awad2021histologicalfindingsafter pages 13-14)

6.3 Suggested ontology terms

• GO biological process: ischemic process; response to hypoxia; neuron death; inflammatory response; angiogenesis.
• CL cell types: spinal motor neuron; astrocyte; microglial cell; vascular endothelial cell.
• UBERON anatomy: spinal cord; anterior horn of spinal cord; thoracic spinal cord; conus medullaris.

(These are mechanistically motivated; ontology IDs were not provided in the retrieved papers.)

7. Anatomical Structures Affected

7.1 Organ/system level

Primary: spinal cord (central nervous system), particularly anterior horn and anterior/lateral white matter supplied by ASA. (zedde2025spinalcordinfarction pages 2-4)

7.2 Localization

Thoracolumbar involvement is common in SCI; one review notes ~65% thoracolumbar region involvement and that cervical infarctions may present more severely with autonomic dysfunction/upper extremity impairment. (zedde2025spinalcordinfarction pages 2-4)

8. Temporal Development

8.1 Onset

Usually acute/hyperacute. Diagnostic reviews emphasize severe deficits developing rapidly (within <12 h) as a core discriminant from inflammatory etiologies. (zedde2025spinalcordinfarction pages 2-4, batsou2023spinalcordischemia pages 3-3)

8.2 Progression

Symptoms often peak quickly (majority by 72 h), but imaging can lag: DWI may detect early lesions before T2 changes in some patients. In a cohort, DWI within 2 days detected lesions in 62.5% (5/8), and a representative case showed DWI positivity on day 2 and T2 changes by day 6. (nagoshi2025imagingcharacteristicsclinical pages 5-8)

9. Inheritance and Population

9.1 Epidemiology

Robust epidemiology is limited; a 2025 review states incidence is “not well documented” and likely underestimated. (zedde2025spinalcordinfarction pages 2-4)

Quantitative estimates (spinal cord infarction, not ASAS-specific): * SCI ~1–2% of all strokes and 5–8% of acute myelopathies. (zedde2025spinalcordinfarction pages 2-4) * Population incidence reported as 3.1/100,000 person-years (95% CI 1.6–7.2) in one study cited in review. (zedde2025spinalcordinfarction pages 2-4)

9.2 Demographics

Vascular risk factors are common but not universal; one review cites 28% with no reported vascular risk factors. (zedde2025spinalcordinfarction pages 2-4)

10. Diagnostics

10.1 Clinical criteria and diagnostic approach

A contemporary review summarizes proposed diagnostic criteria for spinal cord infarction that are directly applicable to ASAS: 1) Rapid development of severe deficits within 12 h; 2) MRI supportive of infarction and excluding compression; 3) Non-inflammatory CSF. Patients may be categorized as definite/probable/possible SCI. (batsou2023spinalcordischemia pages 3-3)

Another contemporary review stresses that “lack of cord compression on MRI is the only mandatory feature” in proposed criteria, highlighting the need to exclude compressive myelopathy. (zedde2025spinalcordinfarction pages 2-4)

10.2 Imaging

MRI findings supporting ASAS include: * axial “owl’s eye” / “snake-eye” anterior horn hyperintensity, * sagittal “pencil-like” anterior T2 hyperintensity, * diffusion restriction (DWI), and often absence of early enhancement. (batsou2023spinalcordischemia pages 1-2, althobaiti2024anteriorspinalartery pages 1-3)

Image evidence: A 2024 case report figure demonstrates ASA territory infarction with “owl’s eye/snake-eye” appearance on T2/DWI. (ferreira2024anteriorspinalcord media 08b84382)

11. Outcome / Prognosis

11.1 Functional outcomes

A review summarizes that favorable functional outcome ~40–50%, and “about half of initially non-ambulatory survivors regained walking.” (batsou2023spinalcordischemia pages 3-3)

In the 19-patient cohort, ASAS predicted poorer ambulatory outcomes: 11/13 (84.6%) of the poor prognosis group had ASA syndrome, whereas Brown–Séquard presentations were associated with better gait outcomes. (nagoshi2025imagingcharacteristicsclinical pages 5-8)

11.2 Prognostic factors

Worse outcomes associate with more severe initial impairment (ASIA A/B), sensory level, and longitudinally extensive MRI lesions. (batsou2023spinalcordischemia pages 3-3)

12. Treatment

12.1 Acute and subacute medical management (evidence-limited)

There is no high-quality ASAS-specific randomized trial base; management is typically extrapolated from vascular neurology and the precipitating cause.

A 2023 review summarized treatment frequencies across series: antiplatelet agents 68%, anticoagulation 8%, blood pressure augmentation 6%, lumbar drain 6%; it also notes limited evidence and uncertainty, particularly for CSF drainage in spontaneous SCI. (batsou2023spinalcordischemia pages 3-3)

12.2 Aortic-repair associated prevention and management (2023–2024 real-world implementation)

The most protocolized “real‑world implementation” literature is peri‑aortic repair spinal cord protection.

Protocol example (Frontiers in Cardiovascular Medicine, Aug 2024): Rosvall et al. reported a prevention protocol for complex EVAR with targets MAP >80 mmHg, Hb >110 g/L, early lower limb reperfusion, and hourly neurologic checks for 36–72 h; prophylactic CSFD used selectively. SCI incidence was 1.3% (juxtarenal) and 6.0% (TAAA); persistent SCI after regression was 0.6% (JRA) and 4.0% (TAAA). https://doi.org/10.3389/fcvm.2024.1440674 (Aug 2024). (rosvall2024adedicatedpreventive pages 1-2)

Protocol example (Vessel Plus, Jan 2024): Sufali et al. reported a multidisciplinary prevention protocol for elective fenestrated/branched repairs with staging in 80%, MAP >80 mmHg, Hb >10 g/dL, routine CSFD, and neuromonitoring. Outcomes: overall SCI 8% (2% transient; 6% permanent), permanent paraplegia 3%, 30‑day mortality 3%, in-hospital mortality 7%, and worse 2‑year survival with SCI (18% vs 69%). https://doi.org/10.20517/2574-1209.2023.139 (Jan 2024). (sufali2024resultsofa pages 1-3)

Expert synthesis (Anesthesia Research, Aug 2024): Torre & Pirri summarize rescue management prioritizing perfusion: increase MAP (cited target >100 mmHg) and transfuse to Hb >10 g/dL, combined with CSFD; they cite neurologic improvement in 57% of delayed deficits and complete resolution in 17% in aggregated reports. https://doi.org/10.3390/anesthres1020010 (Aug 2024). (torre2024enhancingneuroprotectionin pages 10-11, torre2024enhancingneuroprotectionin pages 8-10)

12.3 Suggested MAXO terms (treatment actions)

• Antiplatelet therapy; Anticoagulation therapy; Blood pressure augmentation; Cerebrospinal fluid drainage; Endovascular aortic repair management; Physical rehabilitation therapy; Bladder catheterization/management. (MAXO IDs not provided in retrieved papers; actions are supported as clinical interventions.) (batsou2023spinalcordischemia pages 3-3, rosvall2024adedicatedpreventive pages 1-2)

13. Prevention

Primary prevention is mainly risk reduction for vascular events and prevention of iatrogenic SCI in high-risk procedures.

Aortic procedure prevention (real-world): Staging extensive repairs, maintaining MAP and Hb targets, collateral bed optimization, neurologic monitoring, and selective/routine CSFD reduce persistent injury rates in modern series. (rosvall2024adedicatedpreventive pages 1-2, sufali2024resultsofa pages 1-3)

14. Other Species / Natural Disease

No naturally occurring ASAS “disease entity” in non-human species was identified in the retrieved evidence set; the translational literature primarily uses induced ischemia models. (awad2021histologicalfindingsafter pages 1-2)

15. Model Organisms

ASAS mechanisms (ischemic anterior spinal cord vulnerability) are modeled using aortic cross-clamp or segmental artery ligation paradigms (mimicking open repair or TEVAR) and photochemical/photothrombotic ischemia models.

15.1 TEVAR-like / segmental artery ligation model (mouse; 2023)

Kelani et al. (Anesthesiology, Jan 2023) ligated five pairs of thoracic intercostal arteries to model TEVAR-associated hypoperfusion. * Spinal cord blood flow drop: thoracic spinal cord mean −68.55% (95% CI −80.23 to −56.87). * Day‑1 paralysis severity distribution: 9.4% severe, 37.5% moderate, 53.1% mild. * Severe paralysis mortality: 83% (15/18) vs moderate 33% and mild 24%. The authors state the model yields variable severity and reversibility resembling clinical variability after aortic repair. https://doi.org/10.1097/ALN.0000000000004515 (Jan 2023). (kelani2023mousemodelof pages 1-3)

15.2 Aortic cross-clamp delayed paralysis model (mouse; 2010)

Awad et al. (Anesthesiology, Oct 2010) developed a murine descending aortic cross-clamp model producing delayed paralysis (24–36 h) with >95% survival through 9 weeks under an optimal protocol (7.5 min clamp at 33°C). It produced severe hindlimb paralysis in 70% (19/27) and mild but permanent deficits in the remainder, enabling long-term mechanistic and therapy studies. https://doi.org/10.1097/ALN.0b013e3181ec61ee (Oct 2010). (awad2010amousemodel pages 1-2)

15.3 Simplified spinal cord ischemia model (mouse; 2010)

Wang et al. (J Neurosci Methods, Jun 2010) reported clamp durations of 0–12 min with “approximately 90% blood flow reduction” in lumbar spinal cord during cross-clamping; 10-min injury produced persistent deficits with 28‑day survival 80% (4/5) in an injured group. https://doi.org/10.1016/j.jneumeth.2010.04.003 (Jun 2010). (wang2010developmentofa pages 1-2)

15.4 Histopathology across species (systematic review; 2021)

A systematic review of aortic cross-clamp models concluded injury is predominantly gray matter, with neuronal degeneration in over two‑thirds of cases and anterior gray matter often worse—consistent with anterior horn vulnerability central to ASAS. https://doi.org/10.1093/jnen/nlab084 (Sep 2021). (awad2021histologicalfindingsafter pages 13-14)

Recent developments & latest research emphasis (2023–2024)

Key 2023–2024 advances in this corpus are pragmatic rather than molecular: 1. Refined diagnostic frameworks emphasizing time to nadir, MRI exclusion of compression, and non-inflammatory CSF. (batsou2023spinalcordischemia pages 3-3) 2. More explicit reporting of DWI utility and radiologic lag, including cohort-level estimates and early DWI detection fractions. (nagoshi2025imagingcharacteristicsclinical pages 5-8) 3. Protocolized spinal cord protection bundles for complex EVAR/branched repairs with specific physiologic targets (MAP/Hb), staging, and neurologic monitoring, with measured reductions in persistent SCI and documentation of risk strata (sex, rupture, renal insufficiency, low MAP). (rosvall2024adedicatedpreventive pages 1-2, sufali2024resultsofa pages 1-3) 4. Translational TEVAR-like murine models (2023) enabling mechanistic study of collateral variability and tissue injury patterns that resemble human TEVAR-related spinal cord injury heterogeneity. (kelani2023mousemodelof pages 1-3)

Current applications and real-world implementations

• ICU protocols after complex aortic repair with hourly neurological checks (36–72 h), MAP and hemoglobin targets, early limb reperfusion, and selective CSF drainage are real-world implementations aimed at reducing permanent neurologic injury. (rosvall2024adedicatedpreventive pages 1-2)
• Multidisciplinary prevention pathways integrating vascular surgery, anesthesiology, neuromonitoring, and neuroimaging for early detection and rescue. (sufali2024resultsofa pages 1-3, torre2024enhancingneuroprotectionin pages 10-11)

Expert opinions / analysis (authoritative sources)

Authoritative review analyses emphasize that SCI/ASAS remains underdiagnosed and lacks strong epidemiology; many cases are misdiagnosed as inflammatory myelopathies, and diagnostic pathways are often incomplete. (zedde2025spinalcordinfarction pages 2-4)

Aortic-surgery neuroprotection reviews stress a physiology-based principle: spinal cord perfusion pressure is approximated by MAP minus CSF pressure, motivating CSFD and permissive hypertension/anemia correction as rescue strategies. (torre2024enhancingneuroprotectionin pages 8-10)

Statistics and data highlights

• SCI population incidence: 3.1/100,000 person-years (review-cited estimate). (zedde2025spinalcordinfarction pages 2-4)
• Time to nadir distribution: <6 h 56.1%, 6–12 h 30.7% (meta-analysis). (batsou2023spinalcordischemia pages 3-3)
• ASA syndrome frequency in a cohort: 12/19 cases. (nagoshi2025imagingcharacteristicsclinical pages 5-8)
• Complex EVAR protocol outcomes (Aug 2024): SCI 1.3% (JRA) and 6.0% (TAAA); persistent SCI 0.6% and 4.0% after regression. (rosvall2024adedicatedpreventive pages 1-2)
• F/B‑EVAR protocol outcomes (Jan 2024): overall SCI 8%, permanent paraplegia 3%. (sufali2024resultsofa pages 1-3)

Visual evidence

The following MRI figure demonstrates classic ASA-territory infarction imaging (including the “owl’s eye/snake-eye” sign) supportive of ASAS diagnosis. (ferreira2024anteriorspinalcord media 08b84382)

Synthesis artifact

Table: This table condenses recent and foundational evidence on anterior spinal artery syndrome, including presentation, causes, diagnostics, prognosis, and current treatment/prevention strategies. It is designed as a quick-reference artifact for knowledge base curation and citation mapping.

Limitations of this report (evidence gaps relative to template)

• Formal MONDO/MeSH/Orphanet/ICD identifiers for ASAS were not found in the retrieved full-text excerpts and would require dedicated ontology lookups beyond the current paper set. (althobaiti2024anteriorspinalartery pages 1-3, sliwa1992ischemicmyelopathya pages 1-2)
• High-quality ASAS-specific randomized evidence for antithrombotic selection (antiplatelet vs anticoagulant) is limited; most recommendations are extrapolated from SCI series or the underlying etiology (e.g., aortic repair context). (batsou2023spinalcordischemia pages 3-3)

Primary-source URLs (examples, with publication dates)

• Rosvall L, et al. Front Cardiovasc Med. Aug 2024. “A dedicated preventive protocol sustainably avoids spinal cord ischemia after endovascular aortic repair.” https://doi.org/10.3389/fcvm.2024.1440674 (rosvall2024adedicatedpreventive pages 1-2)
• Sufali G, et al. Vessel Plus. Jan 2024. “Results of a multidisciplinary spinal cord ischemia prevention protocol…” https://doi.org/10.20517/2574-1209.2023.139 (sufali2024resultsofa pages 1-3)
• Torre DE, Pirri C. Anesthesia Research. Aug 2024. “Enhancing Neuroprotection in Cardiac and Aortic Surgeries: A Narrative Review.” https://doi.org/10.3390/anesthres1020010 (torre2024enhancingneuroprotectionin pages 10-11)
• Kelani H, et al. Anesthesiology. Jan 2023. “Mouse Model of Spinal Cord Hypoperfusion…” https://doi.org/10.1097/aln.0000000000004515 (kelani2023mousemodelof pages 1-3)
• Zedde M, et al. J Clin Med. Feb 2025. “Spinal Cord Infarction: Clinical and Neuroradiological Clues…” https://doi.org/10.3390/jcm14041293 (zedde2025spinalcordinfarction pages 2-4)

References

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