Study guide
21.4 Spinal Cord Infarction (03.G)
ABIM Neurocritical Care Subspecialty Certification Exam
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1 Introduction & Exam Overview
1.1 Current Exam Facts 1.2 Eligibility, Practice Pathway, and the IM Training Route 1.3 Format, Scoring, Pearson VUE, and Score Reports 1.4 How to Use This Independent Study Guide
2 ICU Neurologic Exam, Cerebral Physiology, and CSF
2.1 Neurological Examination in the ICU 2.2 Cerebral Physiology, ICP, CBF, and Autoregulation 2.3 CSF Physiology
3 Core Neuropharmacology
3.1 Osmotic Agents 3.2 Anti-Seizure Drugs 3.3 Anesthetics, Sedatives, Analgesia, and Paralytics 3.4 Antihypertensives, Vasopressors, and Inotropes
4 Reperfusion Drugs, Airway, and Ventilation
4.1 Thrombolytics, Anticoagulants, and Antiplatelets 4.2 Reversal of Anticoagulation After Acute Hemorrhage 4.3 Airway Management and Tracheostomy 4.4 Mechanical Ventilation
5 Hemodynamics and Shock
5.1 Hemodynamic Monitoring 5.2 IABP, Temporary VADs, LVAD, and ECMO 5.3 Diagnosis and Management of Shock
6 Nutrition, Temperature, and ICU Prophylaxis
6.1 Nutrition (01.J) 6.2 Temperature Control (01.K) 6.3 ICU Prophylaxis, Delirium, and Early Mobility (01.L)
7 General Trauma
7.1 Emergency Evaluation of Polytrauma, Chest, and Abdominal Trauma 7.2 Long-Bone Fractures and Fat Embolism 7.3 Burns, Electrical Injury, and Hanging/Strangulation
8 Pulmonary Critical Care
8.1 Pulmonary Physiology and ARDS (01.N.1–2) 8.2 PE, Pneumonia, and Pulmonary Edema (01.N.3, 7–8) 8.3 COPD, Asthma, PAH, and Bronchoscopy Basics (01.N.4–6, 9)
9 Cardiovascular Critical Care
9.1 Cardiovascular Physiology, Stress Cardiomyopathy, ACS, and Valves 9.2 Arrhythmias and Pacing 9.3 Acute Aortic Dissection and Cardiac Ultrasound
10 Renal and Infectious Disease
10.1 AKI, RRT, and Renal Drug Dosing 10.2 Acid-Base and Electrolyte Disorders 10.3 Severe Sepsis, Septic Shock, and Infective Endocarditis 10.4 Antimicrobial Use and Infection in the Immunosuppressed
11 Endocrine and Salt-Water Disorders
11.1 Pituitary Apoplexy, DI, and Panhypopituitarism (01.R.1–4) 11.2 SIADH and Cerebral Salt Wasting (01.R.5–6) 11.3 Thyrotoxicosis, Myxedema, Adrenal Crisis, and Dysglycemia (01.R.7–9)
12 Gastrointestinal Critical Care
12.1 GI Physiology, Acute Abdomen, Bleed, Ileus, and Perforation (01.S.1–5) 12.2 Mesenteric Ischemia and Abdominal Compartment Syndrome (01.S.6–7) 12.3 Fulminant Liver Failure, Cirrhosis Decompensation, and Hepatic Dosing (01.S.8–10)
13 Hematologic Disorders
13.1 Anemia, Transfusion, Thrombocytopenia, Coagulopathy, and DIC (01.T.1–4) 13.2 VTE in the Neuro ICU (01.T.5) 13.3 Chemo/Immune, SCT, CAR-T, Sickle Cell, and TMA (01.T.6–10)
14 Neuroimaging
14.1 CT of Brain and Spine 14.2 MRI and CT/MR Perfusion 14.3 Noninvasive Angiography and Catheter Angiography
15 EEG, EMG, and CSF Analysis
15.1 EEG, Standard and Processed (02.B) 15.2 Basic EMG Interpretation (02.G) 15.3 CSF Analysis (02.H)
16 ICP, TCD, and Multimodality Monitoring
16.1 ICP Monitoring (02.C) 16.2 Transcranial Doppler (02.D) 16.3 Brain-Tissue Oxygen and Multimodality Monitoring (02.E–F)
17 Brain Death and Bedside Procedures
17.1 Brain Death Prerequisites and Clinical Exam (02.I) 17.2 Apnea Testing and Ancillary Studies (02.I) 17.3 Vascular Access, Thoracic Echo, and Lung Ultrasound (02.J–L)
18 Coma, Anoxia, and Intracranial Hypertension
18.1 Coma and Other States of Altered Consciousness (03.A) 18.2 Global Anoxia-Ischemia and Post-Resuscitation Encephalopathy (03.A.1) 18.3 Toxidromes, ICU Delirium, and Hypertensive Encephalopathy (03.A.2–4) 18.4 Intracranial Hypertension as a Disease State (03.B)
19 Acute Ischemic Stroke
19.1 IV Reperfusion Therapy (03.C.3) 19.2 Mechanical Thrombectomy Windows and Imaging Selection (03.C.3) 19.3 Malignant Hemispheric Infarction and Basilar Artery Occlusion (03.C.1–2)
20 Intraparenchymal Hemorrhage
20.1 Intracerebral Hematoma (03.D.1) 20.2 Cerebellar Hematoma (03.D.2) 20.3 Intraventricular Hemorrhage (03.D.3)
21 SAH, CVST, and Spinal Cord Infarction
21.1 Aneurysmal Subarachnoid Hemorrhage (03.E.1) 21.2 Non-Aneurysmal SAH (03.E.2) 21.3 Cerebral Venous Sinus Thrombosis (03.F) 21.4 Spinal Cord Infarction (03.G)
22 Vascular Anomalies and Traumatic Brain Injury
22.1 Unruptured Aneurysm, Cavernoma, AVM, and Dural AVF (03.H) 22.2 Diffuse Axonal Injury and Cerebral Contusions (03.I.1–2) 22.3 Epidural Hematoma, Subdural Hematoma, and Penetrating Injury (03.I.3–4, 7) 22.4 Arterial Dissection and Carotid-Cavernous Fistula (03.I.5–6)
23 Spine, Hydrocephalus, and CNS Infection
23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J) 23.2 Unstable Spine Fractures (03.K) 23.3 Hydrocephalus and CSF Diversion (03.L) 23.4 Acute CNS Infections (03.M)
24 Seizures and Neuromuscular Emergencies
24.1 Status Epilepticus and Seizures (03.N) 24.2 Guillain-Barré Syndrome (03.O.1) 24.3 Myasthenic Crisis (03.O.2) 24.4 Motor Neuron Disease, Acute Myopathies, Rhabdomyolysis, and CINM (03.O.3–6)
25 Inflammatory Disease, Neuro-Oncology, and Special Populations
25.1 Fulminant Demyelinating Diseases (03.P) 25.2 Autoimmune Encephalitis and Acute Autonomic Hyperactivity (03.Q–R) 25.3 Neuro-Oncology and Treatment Complications (03.S) 25.4 Pregnancy/Post-Partum, Post-Transplant, and Pediatric Patients (03.T–U)
26 Neurosurgical and Perioperative Complications
26.1 Postoperative Seizures, Hemorrhage, Ischemia, and Hyperperfusion (04.A, C, D, H) 26.2 Infection, CSF Leak, and Pneumocephalus (04.B, E, F) 26.3 Complications of EVD and Lumbar Drain (04.G, I)
27 Ethics, Prognostication, and Organ Donation
27.1 Communication, Decision-Makers, Advance Directives, and DNR (05.A, B, G) 27.2 Uncertainties of Prognostication and the Self-Fulfilling Prophecy (05.C) 27.3 Palliative Care, Withdrawal, Withholding, and Futility (05.D–F) 27.4 Donation After Cardiac Death and Care of the Organ Donor (05.H–I)
21.4 Spinal Cord Infarction (03.G)
Key Takeaways Explain This Topic AI
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.
Last updated: September 2026
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.