23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J)

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 OpenExamPrep 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.

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:

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.

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.