Spinal Motion Restriction

In depth

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Anatomy, tracts and cord syndromes

The cord ends at the conus medullaris at about L1–L2 in adults; below it lie nerve roots (the cauda equina), so a low lumbar injury gives lower motor neuron signs: flaccid weakness and lost reflexes. Injuries cluster at C4–C6 and the thoracolumbar junction (T11–L2). Older adults fracture C1–C2, often the odontoid, in ground-level falls; ankylosing spondylitis makes the spine a brittle lever; children under about 8 injure C1–C3 (large head, lax ligaments).

The anterior spinal artery supplies the anterior two-thirds of the cord, the posterior spinal arteries the dorsal columns. The artery of Adamkiewicz (usually left-sided, T9–T12) feeds the lower cord, and the mid-thoracic cord is a watershed, so hypotension or aortic clamping can cause anterior cord ischemia. Sympathetic outflow leaves the cord at T1–L2 (cardiac accelerators T1–T4); injury above about T6 cuts brain control of the splanchnic vascular bed, the basis of neurogenic shock and autonomic dysreflexia.

Exams explain central cord syndrome by medial arm fibers in the corticospinal tract; anatomists now doubt that lamination and credit the tract's role in fine hand movement (Lemon and Morecraft 2023).

The ASIA (ISNCSCI) examination

The International Standards for Neurological Classification of SCI (ISNCSCI, revised 2019) define level and completeness. Grade 10 key muscles per side from 0 to 5 (0 none, 1 flicker, 2 full range without gravity, 3 against gravity, 4 some resistance, 5 normal; total 100). Score light touch and pinprick at 28 dermatomes per side (0 absent, 1 altered, 2 normal), then test deep anal pressure (DAP) and voluntary anal contraction (VAC).

The neurological level of injury (NLI) is the lowest segment with normal sensation and antigravity strength (grade 3 or better) on both sides, with everything above it normal. Completeness depends only on sacral sparing: any S4–S5 sensation, DAP or VAC makes the injury incomplete. Consortium 2008 bases a preliminary prognosis on an exam within 72 hours; sedation, intoxication and spinal shock can make earlier exams look worse.

From immobilization to motion restriction

Immobilization spread with EMS in the 1970s and shared the credit when most patients began reaching SCI centers with incomplete rather than complete injuries; AANS/CNS 2013 also cited estimates that 3–25% of cord injuries occur after the initial trauma. No randomized trial has tested it. In Hauswald 1998, 120 Malaysian patients carried without devices had less disabling neurologic injury than 334 immobilized New Mexico patients (odds ratio 2.03 for disability with immobilization). In penetrating trauma (Haut 2010, 45,284 patients) immobilized patients died twice as often (14.7% vs 7.2%): one extra death per 66 immobilized, one possible benefit per 1,032.

Boards hurt: all 21 volunteers in one study had pain within 30 minutes, and whole-body immobilization cut respiratory function by about 15% (AANS/CNS 2013 review). That guideline already advised against immobilizing alert, sober patients without pain, tenderness, deficit or distracting injury, or patients with penetrating trauma; the 2018 ACS-COT/ACEP/NAEMSP statement made spinal motion restriction the standard (criteria on the one-pager). A 2025 NAEMSP review argues for fewer collars still; 2026 letters, including an ACS-COT perspective, keep the debate open.

NEXUS (Hoffman 2000, 34,069 blunt-trauma patients) skips cervical imaging only if all five hold: no midline tenderness, no focal deficit, normal alertness, no intoxication, no painful distracting injury. It missed 8 of 818 injuries (99.6% sensitive for significant injury) but was only 12.9% specific. The Canadian C-spine Rule (Stiell 2001, 8,924 alert, stable adults) images age ≥65, paresthesias or a dangerous mechanism (fall from 3 ft or 5 stairs, axial load, high-speed or rollover crash, ejection, motorized recreational vehicle, bicycle collision); a patient with a low-risk factor (such as a simple rear-end crash or walking since the injury) who can actively rotate 45° each way needs no imaging. Head to head (Stiell 2003, 8,283 patients) it beat NEXUS on sensitivity (99.4% vs 90.7%) and specificity (45.1% vs 36.8%).

Obtunded patients cannot be cleared clinically: EAST 2015 conditionally recommends removing the collar after a negative high-quality cervical CT alone, though some centers still require MRI. CT reformats of the chest, abdomen and pelvis usually clear the thoracolumbar spine. Ask daily whether the spine is cleared; every collar-day adds skin and airway risk.

Log roll, transfers and collar care

Moving a patient with an uncleared or unstable spine is a team job. Consortium 2008 suggests four people for a transfer: one at the head calling the count, two for trunk and limbs, one for the slide board or device. Log rolling moves the lumbar spine sideways (AANS/CNS 2013 review), one reason EMS guidance prefers lift-and-slide or a scoop.

1. Prepare: bed flat, suction on, lines slack, analgesia given, plan explained.
2. Head: hold both sides of the head or use a trapezius grip; keep nose, sternum and navel aligned; give every command.
3. Roll as one unit, shoulders and hips together, a pillow between the knees.
4. Inspect the back, sacrum and posterior collar; change linen; roll back on the same count.
5. Recheck motor and sensory function after every major move.
6. Until the thoracolumbar spine is cleared, raise the head with reverse Trendelenburg, not by bending the bed.

Collar care takes two people: one holds the head in line while the other opens the front, cleans and dries the skin, checks occiput, chin, jaw and clavicles, and changes the pads. Replace a one-piece extrication collar with a padded collar if clearance is delayed; skin breakdown can start within 48 hours (AANS/CNS 2013). In flight, a vacuum mattress softens as cabin altitude rises: recheck and re-evacuate it.

Spinal shock and neurogenic shock

Spinal shock is neurologic, not circulatory: tone, reflexes, sensation and movement vanish below the injury. Ditunno 2004 describes four phases: areflexia (day 0–1), return of cutaneous reflexes such as the bulbocavernosus (days 1–3), early hyperreflexia (1–4 weeks) and spasticity (1–12 months). The bulbocavernosus reflex (anal contraction when the glans or clitoris is squeezed or the catheter tugged) classically marks the end of spinal shock.

Neurogenic shock is hemodynamic: lost sympathetic tone dilates arterioles and pools venous blood, and unopposed vagal tone slows the heart. It was present on arrival in 19.3% of isolated cervical cord injuries (Guly 2008; SBP <100 with HR <80). In Lehmann 1987 all 31 patients with severe cervical injury had bradycardia, peaking about day 4 and resolving in 2–6 weeks; 16% had a primary cardiac arrest.

Cord injury hides bleeding (no pain or guarding below the level, blunted heart rate, warm skin), so image the chest, abdomen and pelvis before blaming the cord (Consortium 2008). Restore volume without overload, then start a vasopressor. Norepinephrine is the usual choice because it adds β1 rate and contractility to α1 tone; phenylephrine can deepen bradycardia; dopamine caused more complications than phenylephrine (69% vs 47%, Inoue 2014). AO Spine 2024 found no SCI data on norepinephrine and made no recommendation on the agent.

AANS/CNS 2013 recommends MAP 85–90 mm Hg for 7 days after acute cervical injury (Level III, uncontrolled series). AO Spine 2024 suggests at least 75–80 but not actively above 90–95 for 3–7 days (weak, very low certainty), without lowering a higher pressure reached unaided. A randomized trial (Sajdeya, JAMA Netw Open 2025; 92 patients, MAP >85–90 vs >65–70 for 7 days) found no neurologic difference at 6 months but more respiratory complications (78% vs 39%) and ventilator days with augmentation; it stopped early and lost 29% to follow-up.

Breathing after high cord injury

The diaphragm (phrenic nerve, C3–C5) supplies about 65% of tidal volume; the intercostals (T1–T11) stiffen and lift the chest wall, and the abdominal muscles (T6–L1) power cough. Up to 74% of patients with acute tetraplegia develop ventilatory failure, and about 95% of AIS A injuries above C5 need ventilation (Velmahos 2003, cited in Consortium 2008).

Failure is often delayed as edema raises the level, secretions build and the diaphragm tires; intubation most often happens on days 3–4 (Berlly and Shem 2007). Trend vital capacity, negative inspiratory force and blood gases from baseline; vital capacity below about 15 mL/kg, NIF weaker than −20 cm H₂O, rising PaCO₂ or a falling trend usually prompts planned intubation. SpO₂ falls late.

Intubate with manual in-line stabilization and the collar front open, by video laryngoscope or awake fiberoptic technique, with fluid, a vasopressor and atropine ready: up to 30% of patients with tetraplegia become hypotensive on induction. Avoid succinylcholine after the first 48 hours, when denervated muscle can release enough potassium to stop the heart (Consortium 2008; other references use 24–72 hours).

Clear secretions with assisted (quad) cough, mechanical insufflation-exsufflation, turning and suctioning. Patients with tetraplegia breathe better flat: vital capacity is 16–28% higher supine than sitting, because abdominal contents hold the diaphragm in a better position, so sit them up in stages with an abdominal binder. Plan early tracheostomy when ventilation will be prolonged (Consortium 2008).

Autonomic dysreflexia

Autonomic dysreflexia (AD) occurs with injuries at or above T6, usually after spinal shock resolves, though early episodes are probably underrecognized (Consortium for Spinal Cord Medicine, PVA 2020). A stimulus below the injury, most often a full bladder or bowel, triggers a reflex sympathetic surge that clamps the splanchnic bed. Baroreflexes slow the heart and flush the skin above the level, but descending inhibition cannot pass the lesion, so systolic pressure can reach 300 mm Hg, risking intracranial hemorrhage, seizures and death.

PVA 2020 defines AD as a systolic rise of more than 20 mm Hg above baseline in adults (15 in children); baseline systolic pressure in these patients is often 90–110, so 140 can be a crisis. Signs: pounding headache, flushing and sweating above the level, nasal congestion, blurred vision, bradycardia; some episodes are silent.

1. Sit up, legs down; loosen clothing, binders and leg-bag straps; BP and pulse every 1–2 minutes.
2. Bladder first: trace the catheter for kinks or a full bag, irrigate gently with 10–15 mL of body-temperature saline and replace it if blocked, or catheterize with 2% lidocaine jelly. No Credé.
3. Systolic ≥150: a fast, short-acting drug, first line 2% nitroglycerin ointment on the chest or back, wiped off as BP falls (no nitrates within 24 h of sildenafil or vardenafil, 48 h of tadalafil); alternatives include nifedipine, hydralazine, captopril, clonidine.
4. Still high: instill lidocaine jelly rectally, wait 3–5 minutes, then check for impaction.
5. Then look further: pressure injury, ingrown nail, fracture, abdominal emergency, labor.
6. Afterward, check for hypotension every 2–5 minutes, monitor at least 2 hours, and document the trigger.

Daily care, VTE and troubleshooting

Series without adequate prophylaxis report thromboembolism in 7–100% of patients, mostly within 3 months. AANS/CNS 2013 recommends prophylaxis for severe motor deficits (Level I) with LMWH, rotating beds or a combination, not low-dose heparin alone, started within 72 hours and continued 3 months (Level II); filters only when anticoagulation fails or is impossible. Compression devices start on arrival; the surgeon times the first LMWH dose against epidural bleeding. A vena cava filter is a relative contraindication to manually assisted cough (Consortium 2008).

Pressure injuries develop in 30–50% of patients in the first month, most often sacral (Consortium 2008). Turn at least every 2 hours with spinal precautions on a pressure-redistribution surface, and check heels, occiput and skin under every collar, brace or splint.

• Temperature: no shivering, sweating or vasoconstriction below the injury; track core temperature, adjust room and fluids.
• Bladder: indwelling catheter until hemodynamically stable, then intermittent catheterization.
• GI: ileus, stress-ulcer prophylaxis, swallow screen before eating, bowel program; an abdominal emergency may show only as shoulder pain, fever, distension or AD.
• Mobility: sit up in stages with binder and stockings; midodrine for persistent orthostatic hypotension (low-quality evidence, PVA 2020).
• Coping: plain information with room for hope, an adapted call bell, depression screening.

Steroids, early surgery and what is unsettled

NASCIS II (Bracken 1990) gave methylprednisolone 30 mg/kg over 15 minutes, then 5.4 mg/kg/h for 23 hours; the primary analysis was negative, and only a post hoc subgroup treated within 8 hours gained about 5 motor points. NASCIS III (1997) found more severe pneumonia with 48 than 24 hours of treatment. AANS/CNS 2013 recommends against methylprednisolone (Level I), citing harm without Class I or II evidence of benefit; AO Spine 2017 kept a 24-hour infusion within 8 hours as a weak option.

STASCIS was not randomized: adjusted odds of a ≥2-grade gain were 2.83 with early surgery, with similar complications (24.2% vs 30.5%). AO Spine 2024 now recommends early surgery (within 24 hours) as an option for adults at any level (strong, moderate evidence) and makes no recommendation on ultra-early surgery. Still unsettled: the MAP target and duration, spinal cord perfusion pressure monitoring (MAP minus intrathecal pressure), the best vasopressor, routine field collars, and neuroprotective drugs such as riluzole, none proven.

Exam pearls

• Central cord (arms worse than legs, hyperextension, older adult) is the most common incomplete injury; Brown-Séquard: same-side paralysis, opposite pain and temperature loss.
• Saddle anesthesia with urinary retention: cauda equina syndrome, emergency MRI and decompression.
• Sacral sparing makes an injury incomplete.
• NEXUS needs all five criteria; the Canadian rule images age ≥65, a dangerous mechanism or paresthesias.
• Neurogenic shock: hypotension, bradycardia, warm dry skin; exclude bleeding, give fluid, then norepinephrine.
• Spinal shock is flaccid areflexia; the returning bulbocavernosus reflex marks its end.
• MAP 85–90 for 7 days is the classic answer (AANS/CNS 2013); AO Spine 2024 suggests 75–80 to 90–95 for 3–7 days.
• C3–C5 keeps the diaphragm alive; trend VC and NIF and expect fatigue on days 3–4.
• Autonomic dysreflexia (T6 or above): sit up, loosen clothing, bladder then bowel; drug if systolic stays ≥150.
• No steroids; decompress within 24 hours; no succinylcholine after 48 hours; VTE prophylaxis within 72 hours for 3 months.