Study guide
23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J)
ABIM Neurocritical Care Subspecialty Certification Exam
Track your progress as you read
Finished sections get a check mark.
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)
23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J)
Key Takeaways Explain This Topic AI
ASIA A is a complete injury: no sacral sparing. Any S4–5 sensation, deep anal pressure, or voluntary anal contraction makes the injury incomplete (ASIA B–D).
Central cord syndrome is the common incomplete pattern in older adults after hyperextension; weakness is worse in the upper limbs, especially the hands.
Neurogenic shock is hypotension plus bradycardia from lost sympathetic outflow, usually at T6 or above. Spinal shock is transient areflexia below the lesion, not a blood-pressure diagnosis.
A mean arterial pressure of at least 85 mm Hg for 7 days after acute traumatic spinal cord injury is common 2013 AANS/CNS practice; the supporting evidence is modest, and AO Spine/Praxis 2024 uses a weaker, wider window.
High-dose NASCIS methylprednisolone is not standard care. The 2013 AANS/CNS cervical SCI update recommends against it because infection, hemorrhage, and other harms outweigh unproven neurologic benefit.
Last updated: September 2026
Acute spinal cord injury (SCI) is a dual emergency: the mechanical injury you cannot undo, and the secondary ischemic injury you can worsen with hypotension, hypoxia, a sitting patient on an unstable neck, or a steroid protocol that trades infection for no reliable recovery. Independent ExamFinch teaching for this ABIM Neurocritical Care topic (content outline 03.J) is pattern recognition plus a few numbers that still appear on one-best-answer items. Name the American Spinal Injury Association ( ASIA ) examination, name neurogenic shock correctly, and do not reach for the National Acute Spinal Cord Injury Study ( NASCIS ) methylprednisolone infusion as if it were 1997.
This section is traumatic cord injury. Vascular cord infarction is a different mechanism and is covered with spinal cord infarction in chapter 21. Do not mix the two stems.
Why the first examination must include the sacrum
The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) , published by ASIA, is the language of SCI trials and of most board stems. You test 10 key myotomes on each side (C5–T1 and L2–S1), light touch and pinprick in 28 dermatomes, and the sacral segments that internists skip: S4–5 sensation , deep anal pressure (DAP) , and voluntary anal contraction (VAC) .
The neurological level of injury (NLI) is the most caudal segment with normal motor and sensory function. Complete versus incomplete is not “can the legs move.” It is sacral sparing .
- ASIA Impairment Scale Meaning What you still have
- A Complete No motor or sensory function in S4–5; no DAP, no VAC
- B Sensory incomplete Sacral sensation preserved; no useful motor below NLI
- C Motor incomplete Motor preserved below NLI, but more than half of key muscles below NLI grade <3
- D Motor incomplete Motor preserved, and at least half of key muscles below NLI grade ≥3
- E Normal Motor and sensory scores normal; used after recovery, not at the scene
A patient with flaccid legs who still feels a pin at the anus is not ASIA A. A patient whose legs twitch from reflex withdrawal but who has a vacant sacral examination may still be complete. Zone of partial preservation is documented in complete injuries for the segments below the NLI that retain some function; it is not a fifth ASIA grade.
Prognosis talks often use a 72-hour examination after resuscitation, not the first chaotic trauma-bay grade. Early ASIA A cervical injuries still have a low chance of walking; ASIA D injuries often do. Do not promise a number the trial never published for that exact patient. Do document sacral sparing, because that one finding rewrites the conversation.
Incomplete cord syndromes you must not swap
Central cord syndrome is the incomplete pattern this outline names, and the one you will see in an older adult who fell chin-up. Hyperextension buckles a stenotic cervical canal. The cord is compressed; the corticospinal fibers serving the hands sit more centrally. Classic bedside picture:
- Upper-limb weakness greater than lower-limb weakness
- Hands and intrinsic muscles hit hardest
- Variable sensory loss, often cape-like or patchy
- Sacral sparing is common (this is incomplete SCI)
- Urinary retention is frequent
Recovery is often walking before fine motor. That is not a reason to skip imaging or to sit the patient in a chair before the neck is cleared. Early surgical decompression for persistent compression, including central cord, is discussed in AO Spine timing documents as a treatment option (STASCIS-era observational data favored decompression within 24 hours for a greater chance of two- to three-grade ASIA improvement). Timing is a spine-surgery decision; your job in the ICU is airway, MAP, and not making the cord ischemic while that decision is made.
Other incomplete patterns still appear as distractors:
- Syndrome Typical mechanism What is lost Relative motor prognosis
- Central cord Elderly hyperextension, stenosis Arms > legs, hands worst Often better than anterior cord
Anterior cord Flexion-compression, anterior spinal artery Motor and pain/temperature; dorsal columns spared Among the worst incomplete patterns
Brown-Séquard Hemisection, penetrating or unilateral facet Ipsilateral motor and proprioception; contralateral pain/temperature a level or two below Often favorable walking
Posterior cord Rare; posterior column trauma Vibration and proprioception Motor may be relatively spared
Spinal cord infarction (chapter 21) can mimic anterior cord. Trauma plus a fracture points here; aortic surgery plus an owl-eye T2 lesion points there.
Spinal shock is not neurogenic shock
Spinal shock is a temporary shutdown of reflex activity below the lesion: flaccid areflexic limbs, absent bulbocavernosus reflex ( BCR ), atonic bladder. It can last hours to weeks. Return of the BCR (squeezing the glans or clitoris, or tugging the Foley, produces anal sphincter contraction) is the traditional marker that spinal shock is ending. If the BCR has returned and there is still no sacral sparing, the injury is more likely truly complete. Do not call a patient “complete” in the first hour solely because everything is flaccid.
Neurogenic shock is a hemodynamic diagnosis. Loss of sympathetic outflow, with unopposed vagal tone, produces hypotension plus bradycardia , typically after injuries at T6 and above (the cardiac accelerator fibers leave the cord in the upper thoracic segments). The skin is often warm and dry below the lesion. This is distributive shock, not a volume diagnosis, but the trauma patient can have both neurogenic shock and bleeding.
- Feature Neurogenic shock Hypovolemic / hemorrhagic shock Spinal shock
- Heart rate Bradycardia or relative bradycardia Tachycardia Not defined by heart rate
- Blood pressure Low Low May be normal
- Skin Warm, dry Cool, clammy Not a skin diagnosis
- Lesion Usually T6 or above Any, if bleeding Any cord level
- Time course Hours to days of vasoplegia Follows blood loss Hours to weeks of areflexia
First move Airway, collar, euvolemia, then pressors Stop bleeding, give blood Protect the cord; re-examine sacral function
Worked contrast: a C5 ASIA B patient with MAP 52 mm Hg and pulse 48/min after a modest 400 mL estimated blood loss is neurogenic shock until proven otherwise. A T12 burst fracture with MAP 52 mm Hg, pulse 130/min, and a tense abdomen is bleeding. Giving only phenylephrine to the second patient, or only more crystalloid to a euvolemic high-cervical patient, is the wrong physiology.
Fill the tank to euvolemia first — these patients still lose blood. Then support MAP with a vasopressor. Norepinephrine is a common first ICU agent because it raises MAP without the pure-alpha reflex bradycardia that phenylephrine can worsen in an already vagotonic patient. Historical dopamine infusions still appear in older stems; they are not required. Avoid succinylcholine for intubation after about 48 hours post-injury (acetylcholine-receptor upregulation, hyperkalemic arrest); that risk lasts for months.
MAP targets: common practice, modest evidence
Secondary injury is ischemic. Avoid systolic pressure below 90 mm Hg . The 2013 American Association of Neurological Surgeons/Congress of Neurological Surgeons ( AANS/CNS ) cervical SCI guideline recommended maintaining mean arterial pressure (MAP) between 85 and 90 mm Hg for 7 days after acute SCI (a level III / low-quality evidence statement built on small series such as Vale and Levi). That number is still what many U.S. neuro ICUs write as a default order, and it is still what many exam items expect you to recognize as common practice .
It is not a randomized, high-certainty target. Augmenting MAP means vasopressors, arterial lines, and pulmonary edema in older adults. The 2024 AO Spine/Praxis hemodynamic guideline, looking at the same thin evidence, issued weak recommendations for a wider MAP window (about 75–80 mm Hg on the low end to 90–95 mm Hg on the high end) for 3 to 7 days , and did not lock a single vasopressor. Independent teaching for this exam: know the 85 mm Hg × 7-day AANS/CNS practice line, say out loud that the evidence is modest, avoid hypotension, and do not treat a 90-year-old with cardiomyopathy to a MAP of 95 mm Hg as if that were a Class I command.
Spinal cord perfusion pressure (MAP minus intrathecal pressure from a lumbar drain) is a research and selected-center tool. It is not required to answer a standard MAP item.
NASCIS steroids are not standard care
NASCIS II (Bracken et al., NEJM 1990) reported a motor benefit for methylprednisolone 30 mg/kg bolus then 5.4 mg/kg/h for 23 hours when started within 8 hours — a secondary analysis, not a clean primary endpoint. NASCIS III added a 48-hour infusion for later presenters. Subsequent reviews documented more infection, gastrointestinal bleeding, hyperglycemia, and no convincing functional win. Methylprednisolone is not FDA-approved for SCI. The 2013 AANS/CNS update recommends against administering methylprednisolone for acute SCI. AO Spine documents likewise do not treat high-dose steroids as required neuroprotection. If a stem offers “start NASCIS-dose methylprednisolone immediately” as the next step in an otherwise routine cervical SCI, that option is the trap.
Airway, C-spine, and the later complication you will see in rehab
Airway and cervical motion restriction start together. Manual in-line stabilization, a well-fitted rigid collar, and a video or fiberoptic view that does not crank the head are the ICU translation. High cervical injuries (C3–C5, phrenic nucleus) and complete injuries above C5 often need early intubation; delayed hypercapnia is not a personality trait. Once the patient is in the ICU, get them off the hard backboard; pressure ulcers start on the transfer mat.
Autonomic dysreflexia is not an admission diagnosis. It appears after spinal shock has receded , typically in injuries T6 and above , when a noxious stimulus below the lesion (distended bladder, fecal impaction, tight clothing, pressure ulcer, labor) triggers a spinal reflex vasoconstriction. The brainstem cannot inhibit it. Blood pressure spikes; baroreceptors then slow the heart, so you see hypertension plus bradycardia , flushing and sweating above the lesion, and pallor below. Sit the patient up, loosen clothes, drain the bladder, disimpact the bowel, and use a rapid antihypertensives such as a nitrate, hydralazine, or nifedipine if pressure stays dangerous. Untreated, this can cause intracranial hemorrhage or seizure. It is the opposite of acute neurogenic shock: same cord level family, opposite vital-sign pair, different time in the illness.
Venous thromboembolism risk is high. Chemoprophylaxis is started as soon as hemostasis allows, often within 72 hours, with duration driven by injury severity and mobility — not by a single calendar rule for every ASIA grade.
A worked trauma-bay sequence
A 78-year-old falls, striking the forehead. Arms are flaccid; legs withdraw to pain; there is perianal pin sensation and DAP. Pulse is 44/min, MAP 58 mm Hg, abdomen soft, FAST negative. This is central cord physiology plus neurogenic shock, not a NASCIS steroid case and not isolated hypovolemia. Collar stays on, the airway is secured without a sniffing-position fight, blood is still typed in case bleeding appears, norepinephrine supports MAP toward the local SCI target (commonly ≥85 mm Hg in AANS/CNS-based orders), CT then MRI define cord and ligament injury, and spine surgery is called for decompression timing. Three weeks later, when the same patient gets a plugged Foley and a systolic pressure of 210 mm Hg with a pulse of 50/min, that is autonomic dysreflexia: sit up, unkink the catheter, do not start a workup for new neurogenic shock.