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Spinal Cord Ischemia

1. Disease Information

2026-05-05
Falcon MONDO:0020688 Model: Edison Scientific Literature 47 citations

1. Disease Information

1.1 What is spinal cord ischemia?

Spinal cord infarction is described as a rare ischemic vascular lesion of the spinal cord (a “rare stroke subtype”) that presents as an acute or hyperacute myelopathy and is diagnostically challenging because early MRI (including DWI) can be normal or equivocal. (dokponou2024spinalcordinfarction pages 1-2, zedde2025spinalcordinfarction pages 10-11)

Direct abstract-supported definition (2024 systematic review): Dokponou et al. describe acute spinal cord infarction as “a rare ischemic vascular lesion” and emphasize difficulty diagnosing it in the acute phase, including that diffusion-weighted MRI may fail to show abnormalities early. (dokponou2024spinalcordinfarction pages 1-2)

1.2 Synonyms / alternative names

Commonly used interchangeable terms in the retrieved recent literature include: - Spinal cord infarction (SCI) (dokponou2024spinalcordinfarction pages 1-2) - Spinal cord ischemia (used both for spontaneous infarction and perioperative ischemic injury) (chen2023prophylacticcerebrospinalfluid pages 1-2) - Ischemic spinal cord injury (especially perioperative/aortic contexts) (torre2025spinalcordprotection pages 10-11) - Ischemic myelopathy (historical/vascular syndromic term; identified in review literature) (dokponou2024spinalcordinfarction pages 7-8)

1.3 Key identifiers (ICD/MeSH/MONDO)

Within the retrieved full-text set, formal ICD-10/ICD-11, MeSH, and MONDO identifiers were not explicitly provided, and thus cannot be asserted from the evidence captured here.

For a knowledge base, spinal cord ischemia/infarction is typically mapped under spinal cord vascular disorders and/or spinal stroke; however, this report does not provide codes without direct evidence from the retrieved sources.

1.4 Evidence sources (individual vs aggregated)

2. Etiology

2.1 Primary causal factors

A. Spontaneous / non-iatrogenic spinal cord infarction

A 2024 systematic review/meta-analysis (876 patients) categorized etiologies as: - Vascular: 44.2% - Traumatic: 14.3% - Infectious: 6.1% - Unknown: 35.5% (dokponou2024spinalcordinfarction pages 3-5)

The same review describes etiologies as spontaneous or iatrogenic and lists common causes including aortic disease, cardioembolism, systemic hypoperfusion, vasculitis, and idiopathic causes, with atherosclerosis commonly implicated. (dokponou2024spinalcordinfarction pages 1-2)

B. Iatrogenic/perioperative spinal cord ischemia (aortic surgery)

Spinal cord ischemia is a feared complication after: - Open descending thoracic/thoracoabdominal aortic repair (nasir2023safetyofcerebrospinal pages 1-3) - Thoracic endovascular aortic repair (TEVAR) and thoracoabdominal endovascular procedures (chen2023prophylacticcerebrospinalfluid pages 1-2)

Mechanistically, these settings involve disruption of spinal cord blood supply, extensive segmental artery coverage, hypoperfusion, embolism, and ischemia–reperfusion injury (particularly after open cross-clamping). (torre2025spinalcordprotection pages 1-2, nasir2023safetyofcerebrospinal pages 6-7)

2.2 Risk factors

Spontaneous spinal cord infarction: vascular risks (reported frequencies)

A 2025 review summarizing cohort evidence reported common vascular risk factors in SCI as: - Hypertension ~40% - Smoking ~30% - Dyslipidemia ~29% - Diabetes ~16% - ~28% without reported vascular risk factors (zedde2025spinalcordinfarction pages 2-4)

However, in the 2024 systematic review/meta-analysis dataset, recorded cardiovascular risk factors were often absent: 66.1% had no recorded cardiovascular risk factors, with hypertension 17.1% and hypertension+diabetes 6.2% among those reported. (dokponou2024spinalcordinfarction pages 3-5)

Peri-TEVAR/aortic risk factors

For TEVAR, risk is increased by procedure- and anatomy-related factors, including extent of aortic coverage and collateral vessel occlusion; a meta-analysis notes reported TEVAR SCI rates range 0–17% in literature, with highest rates in thoracoabdominal aneurysm procedures. (chen2023prophylacticcerebrospinalfluid pages 1-2)

2.3 Protective factors

The retrieved evidence is strongest for perioperative protective strategies (rather than host protective factors). Key physiology-guided protective principle: maintaining spinal cord perfusion pressure (SCPP) by supporting arterial pressure and reducing CSF pressure when needed. (torre2025spinalcordprotection pages 10-11, nasir2023safetyofcerebrospinal pages 6-7)

2.4 Gene–environment interactions

No gene–environment interaction evidence specific to spinal cord ischemia/infarction was identified in the retrieved sources.

3. Phenotypes

3.1 Core clinical features and frequencies

From a 2025 clinical-neuroradiological review synthesis: - Motor deficits: 92% - Sensory deficits: 85% - Autonomic dysfunction: 76% - Pain: 70% (zedde2025spinalcordinfarction pages 6-8)

From a 2024 systematic review/meta-analysis (876 patients), pooled phenotype frequencies included: - Hemiplegia 23.2% - Paraplegia 21.7% - Tetraplegia 14.8% - Paraparesis 8.9% - Respiratory dysfunction 11.9% - Swallowing disturbance 7.6% - Asymptomatic 11.9% (dokponou2024spinalcordinfarction pages 3-5)

Pain (including radicular/spinal pain) was reported in 68.6% in the 2024 review’s synthesis. (dokponou2024spinalcordinfarction pages 7-8)

3.2 Temporal development

Time to nadir (time from onset to maximal deficit) is a key discriminator for diagnosis. - 2024 meta-analysis: <6 h (56.1%), 6–12 h (30.7%), 12–72 h (5.4%), >72 h (7.8%). (dokponou2024spinalcordinfarction pages 3-5) - 2025 review synthesis: pooled data suggesting ~81% reach nadir within 12 h (with an additional breakdown in some syntheses), supporting a hyperacute pattern typical of spinal cord infarction. (zedde2025spinalcordinfarction pages 8-10)

3.3 HPO term suggestions (non-exhaustive)

Based on the reported phenotypes: - Paraplegia (HP:0003401) / Paraparesis (HP:0001258) / Tetraplegia (HP:0003300) (dokponou2024spinalcordinfarction pages 3-5) - Sensory impairment (HP:0003401 is motor; for sensory: consider HP:0000769 abnormality of sensation; map more precisely to pain/temperature loss when curated) (zedde2025spinalcordinfarction pages 6-8) - Neuropathic pain (HP:0007018) / Pain (HP:0012531) (zedde2025spinalcordinfarction pages 6-8) - Autonomic dysfunction (HP:0002459) including bladder dysfunction (HP:0000010) (dokponou2024spinalcordinfarction pages 7-8) - Dysphagia (HP:0002015) (dokponou2024spinalcordinfarction pages 3-5) - Respiratory distress/failure (HP:0002098) (dokponou2024spinalcordinfarction pages 3-5)

(Exact HPO IDs should be validated during knowledge base curation; the above are suggested mappings consistent with the phenotype descriptions.)

4. Genetic/Molecular Information

4.1 Causal genes and pathogenic variants

Spinal cord ischemia/infarction is not primarily a monogenic disorder in the retrieved evidence, and no specific causal genes/variants were identified.

4.2 Molecular and cellular mechanisms (pathophysiology)

Causal chain (spontaneous and perioperative)

1) Upstream triggers - Arterial occlusion/embolism, aortic disease/dissection, vertebral artery dissection, systemic hypoperfusion/hypotension, perioperative segmental artery coverage or cross-clamping (dokponou2024spinalcordinfarction pages 1-2, torre2025spinalcordprotection pages 1-2)

2) Perfusion failure and threshold physiology - Spinal cord perfusion pressure (SCPP) is conceptualized as MAP − CSF pressure; lowering intrathecal CSF pressure (e.g., via CSF drainage) and/or raising MAP can increase SCPP. (nasir2023safetyofcerebrospinal pages 6-7, torre2025spinalcordprotection pages 10-11)

3) Tissue vulnerability and vascular territories - Anterior spinal artery (ASA) territory ischemia affects anterior horns/corticospinal/spinothalamic pathways, producing motor deficits, pain/temperature loss, and autonomic dysfunction; posterior spinal artery involvement more strongly affects vibration/proprioception modalities. (zedde2025spinalcordinfarction pages 6-8)

4) Downstream molecular injury cascades In aortic-surgery focused synthesis, secondary injury mechanisms include: - Glutamate excitotoxicity - Oxidative stress / reactive oxygen species (ROS) - Mitochondrial dysfunction - Blood–spinal cord barrier disruption - Inflammation - Calcium influx These are highlighted especially for ischemia–reperfusion contexts (open repair) and for sustained hypoperfusion contexts (TEVAR). (torre2025spinalcordprotection pages 1-2, torre2025spinalcordprotection pages 2-4)

GO term suggestions (biological processes; examples)

  • Response to hypoxia (GO:0001666)
  • Ischemia–reperfusion injury (often curated via related GO terms such as response to oxidative stress GO:0006979)
  • Glutamate receptor signaling pathway (GO:0007215)
  • Mitochondrial dysfunction/mitochondrial depolarization (use appropriate GO mitochondrial process terms during curation)
  • Inflammatory response (GO:0006954)
  • Regulation of blood–brain barrier / blood–spinal cord barrier (curation may use BBB-related GO terms as proxy)

CL term suggestions (cell types)

5. Environmental Information

Spinal cord ischemia/infarction is most strongly linked in the retrieved evidence to: - Iatrogenic/surgical exposures (open aortic repair, TEVAR) (chen2023prophylacticcerebrospinalfluid pages 1-2, nasir2023safetyofcerebrospinal pages 1-3) - Hemodynamic exposures (hypotension/hypovolemia as hypoperfusion drivers) (torre2025spinalcordprotection pages 2-4)

No specific toxin/pollution/occupational exposures were identified in the retrieved sources.

6. Mechanism / Pathophysiology

6.1 Integrated mechanism summary

Aortic-surgery focused synthesis emphasizes the collateral network concept for cord perfusion (segmental arteries plus proximal/distal contributors), and notes two injury patterns: - Ischemia–reperfusion injury (more typical after open repair/cross-clamping) - Sustained hypoperfusion/energy failure (typical of TEVAR due to segmental artery coverage) (torre2025spinalcordprotection pages 2-4)

6.2 Biomarkers / molecular profiling (limited but emerging)

A prospective observational cohort (TURBO; NCT04523909) leverages standard-of-care lumbar drains to measure perioperative CSF inflammatory markers (e.g., IL6, IL8, IL10, MCP-1) and neural injury markers (NFL, S100B, GFAP, UCHL1, NSE), aiming to characterize neuroinflammatory trajectories in thoracic aortic surgery patients. (NCT04523909 chunk 1)

7. Anatomical Structures Affected

7.1 Organ/tissue level

7.2 Vascular territories

7.3 Subcellular / compartment suggestions (hypothesis-supporting)

Given oxidative stress/mitochondrial dysfunction emphasis, mitochondrion (GO:0005739) is a plausible key compartment for injury cascades in ischemia–reperfusion contexts. (torre2025spinalcordprotection pages 2-4)

8. Temporal Development

8.1 Onset pattern

8.2 Course and recovery

Functional outcomes can improve substantially in aggregate: Dokponou et al. report median mRS improving from 3 at admission to 1 at ~12 months in pooled data. (dokponou2024spinalcordinfarction pages 1-2)

9. Inheritance and Population

9.1 Epidemiology

Spontaneous spinal cord infarction

A 2025 review synthesis reports: - SCI estimated at ~1–2% of all strokes and 5–8% of acute myelopathies - Population incidence estimates ~1.5–3.1 per 100,000 person-years (zedde2025spinalcordinfarction pages 2-4)

A 2024 systematic review reiterates rarity and estimates ~0.3–1% of all strokes. (dokponou2024spinalcordinfarction pages 1-2)

Peri-TEVAR spinal cord ischemia

A 2023 meta-analysis (40 studies; n=4,793) estimated pooled TEVAR spinal cord ischemia incidence: - Overall 3.5% (95% CI 2.6–4.4) - Immediate 1.3% - Delayed 1.9% (chen2023prophylacticcerebrospinalfluid pages 6-7)

For TEVAR in type B aortic dissection specifically, a 2024 systematic review (34 studies; n=2,749) reported pooled permanent SCI 2.0% (95% CI 1.0–3.0) and temporary SCI 1.0% (95% CI 0.0–1.0). (zheng2024systematicreviewof pages 1-2)

10. Diagnostics

10.1 Imaging and diagnostic pathway

A 2025 review emphasizes that MRI is central but may be negative early; DWI can help but is imperfect. - Initial MRI abnormal in ~75% (review synthesis), yet up to ~50% of T2 images may be negative within 24 h and a material fraction can have normal initial MRI despite severe deficits. (zedde2025spinalcordinfarction pages 8-10) - DWI is recommended with ADC confirmation; DWI restriction often appears early (reported from the third hour) and ADC may normalize after ~7 days. (zedde2025spinalcordinfarction pages 10-11)

Typical MRI patterns: - Axial “owl’s eyes” sign (central gray matter) and sagittal “pencil-like” anterior cord hyperintensity (zedde2025spinalcordinfarction pages 8-10) - In one pooled dataset, owl’s-eye T2 finding was reported in 48.2% (dokponou2024spinalcordinfarction pages 3-5)

Recommended acute workup in suspected infarction includes emergent CTA chest/abdomen to exclude aortic pathology followed by ischemia-sensitive spinal MRI sequences (DWI/ADC). (zedde2025spinalcordinfarction pages 8-10)

10.2 CSF/labs

CSF is typically non-inflammatory, reported as non-inflammatory in 92% in review synthesis. (zedde2025spinalcordinfarction pages 6-8)

10.3 Differential diagnosis

Important mimics include compressive causes such as spinal epidural or intramedullary hematoma (cord compression). (dokponou2024spinalcordinfarction pages 1-2)

11. Outcome / Prognosis

11.1 Functional outcomes

In pooled data, functional improvement over months is common: - Median mRS improved from 3 at admission to 1 at ~12 months (Dokponou 2024 synthesis). (dokponou2024spinalcordinfarction pages 1-2)

11.2 Mortality

In open aortic repair series with CSF drainage (n=132), in-hospital mortality was 7.6%. (nasir2023safetyofcerebrospinal pages 1-3)

12. Treatment

12.1 Spontaneous spinal cord infarction (medical/supportive)

In the 2024 pooled analysis, the most common management was medical treatment plus physiotherapy (68.9%), with surgical decompression used in 22.8%. (dokponou2024spinalcordinfarction pages 3-5)

MAXO suggestions (to be validated in ontology mapping): - Rehabilitation therapy / physiotherapy - Supportive care - Surgical decompression (when indicated by compressive pathology or selected cases)

12.2 Perioperative prevention and management in aortic surgery

Core principle: preserve spinal cord perfusion pressure and collateral circulation. - SCPP concept: SCPP = MAP − CSF pressure (nasir2023safetyofcerebrospinal pages 6-7) - Strategies: CSF drainage, permissive/induced hypertension, distal aortic perfusion, staged repair, neuromonitoring, collateral preservation/revascularization. (torre2025spinalcordprotection pages 1-2, torre2025spinalcordprotection pages 18-18)

CSF drainage evidence (2023–2024)

In open DTAA/TAAA repair series (Nasir 2023), permanent paraplegia was 3.0% with routine CSF drainage, with CSF drain complications 19% overall (mostly minor) but including serious hemorrhagic events. (nasir2023safetyofcerebrospinal pages 1-3, nasir2023safetyofcerebrospinal pages 6-7)

Guidelines / expert synthesis (aortic surgery)

A 2025 expert review summarizes that guideline support is strongest for open TAAA and more conditional for high-risk endovascular procedures (e.g., EACTS/STS 2024 strong recommendation for open TAAA; consider prophylactic drainage for high-risk endovascular cases). (torre2025spinalcordprotection pages 10-11)

MAXO suggestions (perioperative aortic contexts): - Cerebrospinal fluid drainage - Blood pressure management / induced hypertension - Distal aortic perfusion - Intraoperative neuromonitoring - Endovascular aortic repair / open aortic repair (procedure ontology mapping)

13. Prevention

13.1 Primary prevention

Not applicable in the conventional public-health sense for spontaneous SCI due to heterogeneous etiologies and rarity; prevention focuses on general vascular risk reduction (hypertension/smoking management) and surgical risk mitigation.

13.2 Secondary/tertiary prevention (perioperative)

In aortic surgery, prevention is protocol-driven, emphasizing physiologic protection (SCPP optimization) and rapid rescue because the window to reverse deficits may be short (often discussed as 1–2 hours in expert synthesis). (torre2025spinalcordprotection pages 10-11)

14. Other Species / Natural Disease

No naturally occurring veterinary syndrome was identified in the retrieved sources; the animal evidence primarily concerns induced experimental models.

15. Model Organisms

15.1 Model systems used

A systematic review of preclinical aortic cross-clamping models reports use of: - Mouse, rat, rabbit, dog, pig, baboon, sheep (awad2021histologicalfindingsafter pages 1-2)

A review of models emphasizes that ischemia duration needed for paralysis scales by species (mice ~9–11 min; dogs/pigs ~45–60 min), and that vascular anatomy differences (e.g., artery of Adamkiewicz/radiculomedullary supply) influence reproducibility and translational validity. (awad2013animalmodelsof pages 20-22, awad2013animalmodelsof pages 1-4)

15.2 Representative models and applications

  • Mouse aortic cross-clamp model producing ischemic spinal cord injury with cross-clamp durations of 3–11 minutes and locomotor outcomes assessed by Basso Mouse Scale. (awad2010amousemodel pages 2-4)
  • Canine endovascular embolic model enabling serial clinical-scanner DWI/ADC characterization; DWI hyperintensity observed within 1 hour and biphasic ADC evolution. (zhang2007temporalevolutionof pages 1-2)

15.3 Key conserved pathology

Across cross-clamp models, injury is predominantly in gray matter, though white matter injury can occur. (awad2021histologicalfindingsafter pages 1-2)

Recent developments and real-world implementations (2023–2024 priority)

A. Diagnostic and clinical characterization consolidation

The 2024 systematic review/meta-analysis provides consolidated, quantitative evidence on time-to-nadir, phenotype distributions, imaging signs (owl’s-eye), management patterns, and mRS improvement. (dokponou2024spinalcordinfarction pages 3-5, dokponou2024spinalcordinfarction pages 1-2)

B. TEVAR spinal cord ischemia prevention evidence update

2023–2024 evidence syntheses converge on a key controversy: routine prophylactic CSF drainage has not shown clear pooled benefit in TEVAR, while carrying non-trivial complication risks; selective/high-risk approaches and protocol standardization remain active areas. (chen2023prophylacticcerebrospinalfluid pages 6-7, zheng2024systematicreviewof pages 1-2)

C. Active clinical research directions (trials)

  • NCT04941157: randomized pilot of prophylactic vs therapeutic CSF drain strategy with SCI endpoint (post-op neurologic deficits) (NCT04941157 chunk 1)
  • NCT04523909: perioperative CSF cytokines and injury biomarkers around thoracic aortic surgery (NCT04523909 chunk 1)
  • NCT04600089: ketamine for opioid-sparing analgesia in TEVAR patients receiving naloxone infusion as an SCI-prophylaxis bundle component (NCT04600089 chunk 1)

Evidence table (structured summary)

Table (click to expand)
Topic Citation (authors, year) PMID/DOI Publication date (month/year) Key quantitative findings Key conclusion/implication URL
Spontaneous spinal cord infarction / general SCI overview Dokponou et al., 2024 DOI: 10.25259/sni_477_2024 09/2024 Systematic review of 117 articles/876 patients; mean age 51.1 ± 19.4 years; 64.4% male; acute spinal cord infarction estimated at ~0.3–1% of all strokes; time to nadir: <6 h 56.1%, 6–12 h 30.7%, 12–72 h 5.4%, >72 h 7.8%; MRI alone used in 64.4%; “owl’s eye” sign 48.2%; T2DWI AUC 0.835 for hyperacute detection; 68.9% received medical therapy + physiotherapy, 22.8% surgical decompression; median mRS improved from 3 at admission to 1 at ~12 months; mortality 13.4% (dokponou2024spinalcordinfarction pages 3-5, dokponou2024spinalcordinfarction pages 1-2, dokponou2024spinalcordinfarction pages 2-3) Rare ischemic myelopathy with hyperacute presentation in most cases; MRI/DWI are helpful but imperfect early; outcomes can improve substantially with diagnosis, supportive care, and rehabilitation. https://doi.org/10.25259/sni_477_2024
Spontaneous spinal cord infarction / epidemiology and incidence Zedde et al., 2025 DOI: 10.3390/jcm14041293 02/2025 Review estimates SCI at ~1–2% of all strokes and 5–8% of acute myelopathies; population incidence ~1.5–3.1 per 100,000 person-years; about 8% in multilevel aortic disease; prevalence may reach up to 33% after thoraco-abdominal aortic surgery; typical age 6th–7th decades; vascular risk factors reported: hypertension 40%, smoking 30%, dyslipidemia 29%, diabetes 16%; ~28% lacked reported vascular risks (zedde2025spinalcordinfarction pages 2-4, zedde2025spinalcordinfarction pages 18-20) SCI is probably under-recognized; rapid onset-to-nadir (<12 h) is a strong diagnostic clue, and epidemiologic burden is likely underestimated. https://doi.org/10.3390/jcm14041293
TEVAR / prophylactic CSF drainage meta-analysis Chen et al., 2023 DOI: 10.21037/acs-2023-scp-17 09/2023 Meta-analysis of 40 studies/4,793 TEVAR patients; pooled SCI incidence 3.5% (95% CI 2.6–4.4), immediate SCI 1.3%, delayed SCI 1.9%; no significant difference with CSFD vs no CSFD for any SCI (OR 1.34, 95% CI 0.88–2.04), transient SCI (OR 1.84, 95% CI 0.95–3.54), or permanent SCI (OR 1.25, 95% CI 0.47–3.30); selective CSFD associated with increased transient SCI (OR 2.08, 95% CI 1.06–4.08); CSFD complications: spinal headache 4.3%, major complications 1.6%, epidural/spinal hematoma 0.9%, intracranial/subdural hemorrhage 0.8%, death 0.6%; perioperative mortality 1.7%, mid-term mortality 4.5% (chen2023prophylacticcerebrospinalfluid pages 1-2, chen2023prophylacticcerebrospinalfluid pages 6-7, chen2023prophylacticcerebrospinalfluid pages 10-14) In endovascular thoracic/thoracoabdominal repair, prophylactic CSFD has not shown clear pooled benefit for reducing SCI and is not benign; patient selection and protocol standardization remain important. https://doi.org/10.21037/acs-2023-scp-17
TEVAR for type B aortic dissection / CSF drainage systematic review Zheng et al., 2024 DOI: 10.1186/s13019-024-02603-3 03/2024 Systematic review of 34 studies/2,749 patients; pooled permanent SCI 2.0% (95% CI 1.0–3.0); temporary SCI 1.0% (95% CI 0.0–1.0); no significant difference in permanent SCI with prophylactic CSFD vs none (2.0% vs 2.0%; P=0.445); no difference between routine vs selective CSFD (P=0.596); 30-day/in-hospital mortality 4.0% with prophylactic CSFD vs 5.0% without (P=0.525); mean Downs and Black score 8.71 (zheng2024systematicreviewof pages 5-7, zheng2024systematicreviewof pages 2-5, zheng2024systematicreviewof pages 1-2) For TEVAR in type B aortic dissection, pooled nonrandomized data do not support a reduction in permanent SCI or short-term mortality from prophylactic CSFD. https://doi.org/10.1186/s13019-024-02603-3
Open descending thoracic/thoracoabdominal aortic repair / CSF drainage safety Nasir et al., 2023 DOI: 10.21037/acs-2023-scp-0121 09/2023 Single-center 17-year series, n=132 with routine CSFD; in-hospital mortality 7.6%; transient paresis 3.8%; permanent paraplegia 3.0%; CSFD complications 19% overall, including persistent CSF leak 7%, blood-tinged CSF 11%, subdural hematoma in 3 patients, spinal cutaneous fistula 1%; survival 86.4% at 1 year, 75.2% at 5 years, 50.9% at 15 years; ACC/AHA recommendation cited as Class I, Level A for open TAAA repair (nasir2023safetyofcerebrospinal pages 1-3, nasir2023safetyofcerebrospinal pages 4-6, nasir2023safetyofcerebrospinal pages 6-7, nasir2023safetyofcerebrospinal pages 3-4) In open DTAA/TAAA repair, CSFD remains a commonly used protective adjunct with accepted complication risk; evidence and guidelines are stronger here than for TEVAR. https://doi.org/10.21037/acs-2023-scp-0121
Guideline/review synthesis for aortic-surgery spinal cord protection Torre & Pirri, 2025 DOI: 10.3389/fcvm.2025.1671350 09/2025 Review cites randomized open TAAA data showing paraplegia/paraparesis 13% without vs 2.6% with CSFD; states 2024 EACTS/STS strongly recommend CSFD for open TAAA replacement (Class I, Level B) and advise considering prophylactic drainage for high-risk endovascular cases (Class IIa, Level C); also notes insufficient evidence for routine prophylactic drainage in endovascular procedures (torre2025spinalcordprotection pages 10-11) Current expert guidance supports CSFD most strongly for open TAAA repair, while high-risk TEVAR decisions should be individualized within bundled spinal cord protection strategies. https://doi.org/10.3389/fcvm.2025.1671350
Trial: prophylactic vs therapeutic drain strategy in endovascular TAAA repair NCT04941157 2022 (registry record) Randomized pilot interventional study; enrollment 20; compares prophylactic CSF drain placement before high-risk endovascular thoracoabdominal aneurysm repair vs selective/therapeutic placement only if SCI develops; primary outcome: rate of postoperative spinal cord ischemia over 1 year, defined as new lower-extremity neurologic deficit, assessed with Muscle Power Scale (NCT04941157 chunk 2, NCT04941157 chunk 1) Directly addresses a major unresolved clinical question: whether pre-emptive drain placement improves neurologic outcomes enough to justify drain-related risk. https://clinicaltrials.gov/study/NCT04941157
Trial: ketamine during TEVAR patients receiving naloxone continuous infusion for SCI prophylaxis NCT04600089 2020 (registry record) Phase 2 randomized double-blind placebo-controlled trial; enrollment 30; ketamine infusion 0.2 mg/kg/h vs saline for 48 h in TEVAR patients receiving naloxone continuous infusion for spinal ischemia prophylaxis; primary outcome cumulative opioid dose over 48 h; secondary outcomes pain scores, delirium (CAM-ICU), uncontrolled hypertension (NCT04600089 chunk 1) Tests an analgesic strategy within an SCI-prevention bundle, addressing the pain/opioid burden introduced by naloxone-based prophylaxis rather than SCI efficacy directly. https://clinicaltrials.gov/study/NCT04600089
Trial: CSF neuroinflammatory biomarkers around thoracic aortic surgery NCT04523909 2017 (registry record) Prospective observational cohort; enrollment 100; serial CSF and blood sampling across 9 perioperative timepoints to measure IL6, IL8, IL10, MCP-1, IL1RA, CX3CL1 and markers including NFL, S100B, GFAP, UCHL1, NSE; lumbar drain placed as standard care to reduce periprocedural spinal cord ischemia risk (NCT04523909 chunk 1) Important translational study for biomarker discovery and mechanistic monitoring; may inform future prediction of perioperative neurologic injury, though it is not an intervention trial for SCI prevention. https://clinicaltrials.gov/study/NCT04523909

Table: This table summarizes recent core evidence on spontaneous spinal cord infarction and perioperative spinal cord ischemia prevention in aortic surgery. It highlights incidence estimates, imaging and outcome data, CSF drainage meta-analyses, guideline interpretations, and ongoing clinical trial directions.

Visual evidence from a key 2023 meta-analysis

Chen et al. (2023) provides forest plots and tables summarizing CSF drainage vs no drainage outcomes and complication rates; these were retrieved as cropped figure/table images, including the main results table, forest plots, and CSF-drain complication table. (chen2023prophylacticcerebrospinalfluid media cf49819c, chen2023prophylacticcerebrospinalfluid media 628d27e4, chen2023prophylacticcerebrospinalfluid media 3b07512f, chen2023prophylacticcerebrospinalfluid media 2ef757c8, chen2023prophylacticcerebrospinalfluid media 0f2ce663)

Limitations of this report (evidence availability)

  • Ontology identifiers (MONDO, MeSH, ICD-10/ICD-11) were not explicitly present in the retrieved full text, so they are not asserted here.
  • PMIDs were not available in the extracted evidence snippets (most sources provide DOIs and journal metadata). All sources are linked via DOI/ClinicalTrials.gov URLs.
  • Some mechanistic claims (e.g., specific cytokine or excitotoxic cascades) appear in expert synthesis rather than primary mechanistic experiments in the retrieved set; preclinical modeling evidence is included to partially address this.

References

  1. (dokponou2024spinalcordinfarction pages 1-2): Yao Christian Hugues Dokponou, Fresnel Lutèce Ontsi Obame, Berjo Takoutsing, Mubarak Jolayemi Mustapha, Arsène Daniel Nyalundja, Moussa Elmi Saad, Omar Boladji Adebayo Badirou, Dognon Kossi François de Paule Adjiou, Nicaise Agada Kpègnon, Alngar Djimrabeye, and Nourou Dine Adeniran Bankole. Spinal cord infarction: a systematic review and meta-analysis of patient’s characteristics, diagnosis accuracy, management, and outcome. Surgical Neurology International, 15:325, Sep 2024. URL: https://doi.org/10.25259/sni_477_2024, doi:10.25259/sni_477_2024. This article has 14 citations and is from a peer-reviewed journal.

  2. (chen2023prophylacticcerebrospinalfluid pages 1-2): Cheng-Hao Jacky Chen, Henry Jiang, and Vinh Dat David Nguyen. Prophylactic cerebrospinal fluid drainage and spinal cord ischemia in thoracic and thoracoabdominal endovascular procedures: a systematic review and meta-analysis. Annals of Cardiothoracic Surgery, 12:392-408, Sep 2023. URL: https://doi.org/10.21037/acs-2023-scp-17, doi:10.21037/acs-2023-scp-17. This article has 13 citations.

  3. (zedde2025spinalcordinfarction pages 10-11): Marialuisa Zedde, Arturo De Falco, Carla Zanferrari, Maria Guarino, Francesca Romana Pezzella, Shalom Haggiag, Gianni Cossu, Rocco Quatrale, Giuseppe Micieli, Massimo Del Sette, and Rosario Pascarella. Spinal cord infarction: clinical and neuroradiological clues of a rare stroke subtype. Journal of Clinical Medicine, 14:1293, Feb 2025. URL: https://doi.org/10.3390/jcm14041293, doi:10.3390/jcm14041293. This article has 16 citations.

  4. (torre2025spinalcordprotection pages 10-11): Debora Emanuela Torre and Carmelo Pirri. Spinal cord protection in open and endovascular aortic surgery: current strategies, controversies and future directions. Frontiers in Cardiovascular Medicine, Sep 2025. URL: https://doi.org/10.3389/fcvm.2025.1671350, doi:10.3389/fcvm.2025.1671350. This article has 3 citations and is from a peer-reviewed journal.

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