21.4 Spinal Cord Infarction (03.G)
Key Takeaways
- Anterior spinal artery syndrome produces bilateral motor loss and bilateral pain/temperature loss with spared dorsal-column vibration and proprioception; it is the most common spinal cord infarct pattern.
- Classic precipitants are aortic surgery or TEVAR, systemic hypotension, aortic dissection, and fibrocartilaginous embolism after a Valsalva or minor axial load in a younger patient.
- Spine MRI with diffusion-weighted imaging can show restriction within hours, but early MRI may be normal — repeat imaging if suspicion stays high. Time to nadir under about 12 hours favors infarct over inflammatory myelopathy.
- After aortic repair, MAP augmentation (often ≥85–90 mm Hg) and CSF drainage to raise spinal cord perfusion pressure are used in prevention and rescue protocols; the 2022 ACC/AHA aortic guideline gives prophylactic CSF drainage Class 1 for high-risk open thoracoabdominal repair.
- Compressive myelopathy (epidural hematoma, abscess, tumor, burst fracture) is a surgical emergency and must be excluded on MRI before you settle on medical management of cord ischemia.
Spinal cord infarction is uncommon compared with cerebral stroke, and that is exactly why it is missed. The patient reports sudden back or chest pain, then cannot move the legs. If you wait for a perfect MRI while an epidural hematoma expands, you have treated the wrong emergency. If you rush a laminectomy on an anterior spinal artery infarct with no compression, you have operated on a vascular cord. This section is the neurointensivist's job: territory, mechanism, imaging timing, perfusion pressure, and the compressive look-alike.
Vascular anatomy you actually use
The anterior spinal artery (ASA) is a single midline vessel running in the anterior median fissure. It supplies the anterior two-thirds of the cord: corticospinal tracts, spinothalamic tracts, and autonomic fibers. Two posterior spinal arteries supply the dorsal columns. Radiculomedullary feeders from the aorta reinforce the ASA; the largest is usually the artery of Adamkiewicz, most often on the left between T8 and L2. Thoracic cord has a watershed personality. Aortic cross-clamp, coverage of intercostals during thoracic endovascular aortic repair (TEVAR), or a hypotensive night in the ICU can drop that watershed below the line.
| Syndrome | What is lost | What is spared |
|---|---|---|
| Anterior spinal artery (Beck) syndrome | Bilateral motor; bilateral pain and temperature; often bowel/bladder; may have spinal shock | Dorsal-column vibration and proprioception |
| Posterior spinal artery | Vibration and proprioception, often patchy | Motor and pain/temperature relatively spared |
| Sulcal (central) / incomplete ASA | Incomplete or asymmetric motor and spinothalamic findings; "man-in-the-barrel" if cervical | Variable |
| Transverse / complete | Everything below the level | Nothing — consider occlusion of both anterior and posterior supply or severe swelling |
Anterior spinal artery syndrome is the pattern the exam wants first: flaccid then spastic paresis, a sensory level to pinprick and temperature, and preserved dorsal-column sensation. Patients can still feel the tuning fork on the toe while they cannot feel a pin on the same dermatome. If vibration is gone together with motor and pain, think complete transverse lesion or compression, not a pure ASA infarct.
A sensory level plus acute bladder involvement is expected. Areflexia in spinal shock lasts hours to weeks before hyperreflexia appears; do not call it Guillain-Barré solely because reflexes are out on day 0 if there is a truncal sensory level and MRI of the cord shows a pencil of T2 change.
Mechanisms: aorta, pressure, and disc
| Mechanism | Typical setting | Notes |
|---|---|---|
| Open or endovascular aortic repair | TAAA, TEVAR, some left-heart bypass | Delayed paraplegia (hours to a few days) is well described when MAP drops or the CSF drain clots |
| Aortic dissection or intramural hematoma | Chest/back pain plus cord syndrome | Treat the aorta; the cord is a downstream victim |
| Systemic hypotension / cardiac arrest | Watershed thoracic cord | May accompany cerebral anoxic injury |
| Atherosclerosis / embolism | Older patients, atrial fibrillation less classic than aortic atheroma | Vertebral-origin cervical ASA infarcts occur |
| Fibrocartilaginous embolism (FCE) | Younger; Valsalva, heavy lift, minor trauma, sometimes childbirth | Nucleus pulposus fragments enter a radicular artery; often cervical or upper thoracic; no aortic scar |
| Vasculitis, cocaine, decompression sickness, hemoglobinopathy | Context-specific | Do not miss infection and inflammation that mimic infarct |
Fibrocartilaginous embolism is the favorite "young athlete after deadlifts" stem. Pain at onset is common. MRI may show a collapsed disc or Schmorl node adjacent to an anterior-cord DWI lesion. There is no clot-retrieval device for FCE; treatment is supportive perfusion pressure and rehabilitation.
MRI: DWI, owl eyes, and the normal early scan
MRI of the spine is the first-line imaging test, and it has two jobs: show ischemia and exclude compression. Sequences that matter:
- Sagittal T2: longitudinally extensive, often "pencil-like," anterior-predominant hyperintensity over multiple levels
- Axial T2: owl-eye or snake-eye hyperintensity in the anterior horns
- Diffusion-weighted imaging (DWI) with ADC: restriction can appear within a few hours, earlier than T2
- Contrast: infarct usually does not enhance early; patchy enhancement later. Intense enhancement plus a compressive mass is not infarct
- Adjacent vertebral-body infarct, rib, or muscle infarct supports an aortic/embolic mechanism
Early MRI can be normal. If the clinical syndrome is ASA and there is no compression, treat as ischemia, keep perfusion up, and repeat MRI in 24–48 hours. A time to nadir of severe deficits under about 12 hours is one of the strongest clinical clues separating infarct from inflammatory myelitis (which more often evolves over many hours to days and may show CSF pleocytosis and patchy enhancement).
Vascular imaging of the aorta (CTA) is part of the workup when dissection or aneurysm is plausible. Spinal catheter angiography is rarely the first test in acute infarct and is more relevant when you are hunting a dural fistula (which usually presents as a progressive myelopathy, not a 10-minute ASA syndrome).
MAP augmentation and CSF drainage after aortic surgery
Spinal cord perfusion pressure is roughly MAP minus CSF pressure (or central venous pressure, whichever is higher). Two levers exist: raise MAP and drain CSF.
The 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease supports hemodynamic optimization and designates prophylactic CSF drainage Class 1, Level A for patients at elevated risk of spinal cord injury during open thoracic and thoracoabdominal aortic repair. Institutional protocols commonly keep MAP at least 85–90 mm Hg (some rescue protocols >90 mm Hg) in the first 48–72 hours, and they drain CSF to a pressure around 10 mm Hg or less to keep spinal cord perfusion pressure near 80 mm Hg. Delayed paraplegia after TEVAR is treated as an emergency: raise MAP, resume or unclamp the drain, correct anemia and hypoxia, and call the aortic team.
These numbers are protocolized aortic-surgery tools. They are reasonable to consider in spontaneous cord infarct as a perfusion strategy (many teams target MAP ≥85 mm Hg by analogy to traumatic cord and aortic protocols), but they are not a thrombolysis substitute and they do not replace surgical decompression when a mass is present. Lumbar drains have complications (infection, overdrainage, subdural hematoma, meningitis); they belong in teams that place them often.
There is no established IV thrombolysis indication equivalent to 4.5-hour alteplase for brain for routine spinal cord infarct. Case reports exist; they are not standard neurocritical care. NASCIS-style high-dose methylprednisolone is not the treatment for ischemic cord any more than it is standard for traumatic cord in current AANS/CNS practice.
Distinguish compressive emergency from infarct
This is the decision that changes the next 30 minutes.
| Feature | Cord infarct | Compressive emergency |
|---|---|---|
| Onset | Hyperacute, often with pain, nadir <12 h | Acute or subacute; may be rapidly progressive |
| Dorsal columns | Often spared (ASA) | Often involved if the thecal sac is crushed |
| MRI | Intramedullary T2/DWI, no extra-axial mass | Epidural hematoma, abscess, disc, tumor, fracture retropulsion |
| Systemic clue | Aortic procedure, hypotension, FCE history | Anticoagulation (epidural hematoma), fever/IVDU (abscess), known cancer |
| Treatment | MAP, CSF drain in aortic protocols, medical | Immediate surgical (or interventional) decompression |
An anticoagulated patient who becomes paraplegic after an epidural injection has an epidural hematoma until MRI proves otherwise. Fever, back pain, and a level in a person who injects drugs is epidural abscess. Metastatic cord compression still gets steroids and surgery/radiation — that is not ASA syndrome. If MRI cannot be obtained instantly, the compressive story plus a level is a spine-surgeon/MRI emergency, not a "watch overnight for owl eyes" plan.
Also separate:
- Guillain-Barré: no truncal sensory level, often albuminocytologic dissociation, nerve-root enhancement, not cord DWI restriction
- Transverse myelitis / NMOSD: hours to days, often enhancing, CSF inflammatory, aquaporin-4 antibodies in the right phenotype
- Watershed cerebral stroke: not a spinal level
ICU course and recovery
Supportive care is the remainder: bladder catheter, bowel regimen, DVT prophylaxis (the paralyzed cord is a clot risk), skin, and ventilator support if the infarct is high cervical (diaphragm, C3–C5). Autonomic dysregulation and spinal shock can drop blood pressure — which is the opposite of what the cord needs. Pain can be severe (spinothalamic and cord dysfunction). Prognosis is often guarded for independent walking when the motor complete lesion persists, but some ASA infarcts, especially incomplete ones and some FCE cases, recover meaningful function. Delayed deficits after aortic repair that reverse with MAP and CSF drainage are the hopeful subset; document the time you raised the pressure.
In practice
A 68-year-old is 8 hours after TEVAR. MAP drifts to 65 mm Hg overnight. At 06:00 the patient cannot move either leg; pinprick is lost to T10; vibration at the toes is intact. This is anterior spinal artery ischemia until proven otherwise. Raise MAP into the protocol range, check the CSF drain, get an urgent MRI to exclude epidural hematoma from the drain, and do not wait for a neurologically complete lesion to "declare." Contrast a 24-year-old who felt a pop while lifting, then developed the same ASA pattern: think fibrocartilaginous embolism, MRI DWI of the cord, no aortic graft, still exclude compression. Contrast a 70-year-old on warfarin with back pain and a complete transverse level including lost proprioception: MRI looking for epidural hematoma, not a 48-hour wait for owl-eye T2.
A patient develops sudden paraplegia after a hypotensive episode. Pinprick and temperature are lost below T8. Vibration and proprioception in the toes are preserved. Which vascular territory does this describe?
An anticoagulated patient becomes paraplegic over 30 minutes with a dense sensory level including loss of proprioception. Which action takes priority over a working diagnosis of spinal cord infarction?
A patient awakens paraplegic 12 hours after open thoracoabdominal aortic aneurysm repair. The CSF drain has not been producing. Which intervention set is used in aortic-surgery spinal cord protection protocols?