Neurology · PANCE / PANRE

Acute Spinal Cord Injury / Compression

Sudden disruption of spinal cord function from trauma, compression, ischemia, or inflammation; outcome depends on completeness of injury and time to decompression.

Also known as: spinal cord injury, SCI, acute spinal cord compression, traumatic spinal cord injury, cord syndrome

Overview

Acute disruption of spinal cord function due to mechanical injury (fracture/dislocation, penetrating trauma), extrinsic compression (epidural abscess, hematoma, metastasis, large disc), vascular insult (anterior spinal artery syndrome, dural AV fistula), or inflammatory/demyelinating disease (transverse myelitis). Severity is classified by the ASIA Impairment Scale (AIS A-E).

Epidemiology

Traumatic SCI incidence ~50-60 per million per year in the US; male predominance ~4:1; bimodal peaks in young adults (motor vehicle, sports, violence) and older adults (falls with cervical stenosis). Non-traumatic compression most often from malignancy (lung, breast, prostate, multiple myeloma, lymphoma).

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Question 1NeurologyMedium
A 60-year-old man reports 8 months of slowly progressive hand clumsiness, difficulty buttoning his shirt, and a stiff, unsteady gait. On examination there is bilateral intrinsic hand muscle weakness, spasticity and hyperreflexia in both legs, an extensor plantar response, and a positive Hoffman sign; vibration sense is diminished in the feet. There are no fasciculations, bulbar symptoms, or cranial nerve deficits. MRI of the cervical spine shows multilevel degenerative disc-osteophyte complexes narrowing the spinal canal with increased T2 cord signal at C3-C5, without an intramedullary syrinx or demyelinating plaques. Which of the following is the most likely diagnosis?
  • ACervical spondylotic myelopathy
  • BMultiple sclerosis
  • CAmyotrophic lateral sclerosis
  • DCervical syringomyelia
Reveal answer & full explanation
Correct answer: A — Cervical spondylotic myelopathy
  • ACervical spondylotic myelopathy
  • BMultiple sclerosis
  • CAmyotrophic lateral sclerosis
  • DCervical syringomyelia

Why Cervical spondylotic myelopathy is correct

  • Cervical spondylotic myelopathy is the most common cause of non-traumatic spinal cord dysfunction in adults over 55 and presents exactly as here: insidious hand clumsiness, intrinsic hand weakness, and a spastic gait.
  • Upper-motor-neuron signs in the legs (spasticity, hyperreflexia, extensor plantar response, Hoffman sign) WITH sensory involvement (diminished vibration) localize a compressive cervical cord lesion.
  • MRI shows multilevel degenerative canal stenosis with T2 cord signal change at C3-C5, and the absence of a syrinx or demyelinating plaques rules out the mimics.
  • Management is timely surgical decompression (anterior cervical discectomy and fusion or laminoplasty) to halt progression.

Why the others are wrong

  • Multiple sclerosis — typically affects younger patients with relapsing optic, brainstem, or spinal demyelination; the MRI shows compressive stenosis and no demyelinating plaques (buzzword-matching on 'cord signal change').
  • Amyotrophic lateral sclerosis — produces mixed upper- and lower-motor-neuron signs but spares sensation and shows fasciculations, not a sensory deficit or cord compression; the diminished vibration sense and compressive MRI exclude it (premature closure on a progressive-weakness picture).
  • Cervical syringomyelia — causes a cape-like dissociated sensory loss and shows a fluid-filled intramedullary cavity on MRI, which is explicitly absent here (confused-with another structural cord lesion).
Question 2NeurologyMedium
A 72-year-old man undergoing evaluation for severe aortic stenosis develops sudden bilateral leg weakness, urinary retention, and loss of pain and temperature sensation below the level of the umbilicus. Proprioception and vibration sense are preserved in both legs. MRI of the spine shows an anterior cord T2 signal change at the T9 level. In addition to treating the underlying cause, which of the following is the most appropriate management?
  • AMean arterial pressure augmentation
  • BTherapeutic anticoagulation
  • CHigh-dose intravenous corticosteroids
  • DEmergent surgical decompression
Reveal answer & full explanation
Correct answer: A — Mean arterial pressure augmentation
  • AMean arterial pressure augmentation
  • BTherapeutic anticoagulation
  • CHigh-dose intravenous corticosteroids
  • DEmergent surgical decompression

Why mean arterial pressure augmentation is correct

  • The presentation is anterior spinal cord syndrome caused by anterior spinal artery ischemia: motor paralysis, loss of pain and temperature sensation, and bladder dysfunction below the lesion, with preserved proprioception and vibration.
  • Proprioception and vibration are preserved because the dorsal columns are supplied by the separate posterior spinal arteries.
  • The anterior two-thirds of the cord is supplied by the anterior spinal artery and is injured by hypoperfusion.
  • Because the injury is ischemic, the cornerstone of management is augmenting spinal cord perfusion by targeting a mean arterial pressure above roughly 85–90 mm Hg and avoiding hypotension, alongside treatment of the underlying cause.
  • Anterior cord syndrome is classically associated with aortic disease, hypotension, and embolic events.

Why the others are wrong

  • B) Therapeutic anticoagulation — Not first-line; the mechanism is typically arterial hypoperfusion or embolism rather than a thrombus requiring systemic anticoagulation, and it carries bleeding risk without proven benefit.
  • C) High-dose intravenous corticosteroids — Tempting because students associate steroids with acute spinal cord injury, but they are not evidence-based for ischemic anterior cord syndrome and are not standard of care here.
  • D) Emergent surgical decompression — Indicated for compressive cord lesions such as epidural hematoma, abscess, or tumor; imaging here shows ischemic signal change without a compressive mass, so there is nothing to decompress.

Additional high-yield points

  • Anterior cord syndrome carries the worst prognosis of the incomplete cord syndromes, underscoring the importance of optimizing perfusion early.
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Risk factors

  • Motor vehicle collision, falls (especially older adults with cervical spondylosis), sports (diving), violence
  • Cervical spondylosis or congenital spinal canal narrowing (predisposes to central cord syndrome)
  • Ankylosing spondylitis (rigid spine fractures with minor trauma)
  • Known malignancy with spine-tropic biology
  • Anticoagulation or coagulopathy (epidural hematoma)
  • IV drug use, immunosuppression (epidural abscess)
  • Vascular risk factors (aortic surgery, atherosclerosis) for anterior spinal artery infarct

Pathophysiology

Primary injury (mechanical disruption, transection, contusion) produces immediate neurologic deficit. Secondary injury — edema, ischemia, glutamate excitotoxicity, oxidative stress, inflammation, apoptosis — extends damage over hours to days. Decompression and stabilization aim to prevent secondary injury and preserve residual function.

Clinical presentation

Symptoms

  • Acute weakness or paralysis below the level of injury
  • Sensory loss with a discrete dermatomal level on the trunk
  • Bowel and bladder dysfunction (retention initially)
  • Neck or back pain at the level of injury
  • Priapism (complete cord injury), respiratory distress (high cervical injury)
  • Specific cord syndromes (see by_subtype)

Signs / physical exam

  • Motor: flaccid weakness in spinal shock phase; later spasticity, hyperreflexia, upgoing toes
  • Sensory: defined level to pinprick and light touch; dissociated loss in central/Brown-Séquard/anterior cord patterns
  • Reflexes: areflexic acutely, hyperreflexic with time (UMN pattern)
  • Autonomic: hypotension and bradycardia (neurogenic shock) with injuries above T6; loss of sphincter tone
  • Priapism (sympathetic disruption)

Classic findings

Discrete sensory level + motor deficit below + bladder retention + back pain after trauma or in a cancer patient.

Differential diagnosis

  • Cauda equina syndrome — Lumbosacral root compression below conus — saddle anesthesia, bladder dysfunction, lower-extremity LMN signs only (see separate entry)
  • Guillain-Barré syndrome — Ascending flaccid weakness, areflexia, no sensory level, albuminocytologic CSF
  • Transverse myelitis — Subacute (hours-days), sensory level, often inflammatory; consider MS, NMO, autoimmune
  • Stroke (anterior cerebral or pontine) — Cortical/brainstem signs, asymmetric, intact spinal exam below lesion
  • Conversion / functional weakness — Inconsistent exam, give-way weakness, preserved bowel/bladder; diagnosis of exclusion after imaging

Diagnostic workup

Diagnostic criteria

ASIA International Standards for Neurological Classification of SCI: motor (key muscles graded 0-5) and sensory (pin-prick and light touch in 28 dermatomes) examination defines the neurological level and AIS grade A (complete) through E (normal).

Labs

  • CBC, CMP, coagulation studies
  • Type and screen
  • Toxicology if trauma context
  • ESR/CRP, blood cultures if infection suspected

Imaging

  • CT cervical/thoracic/lumbar spine — first-line trauma imaging for bony injury
  • MRI whole spine with and without contrast — modality of choice for cord and soft tissue evaluation, especially in compression, abscess, hematoma, malignancy, or transverse myelitis
  • CT angiography if vertebral artery injury suspected (penetrating, foramen transversarium fracture)

Treatment

First-line

  • ABCs — high cervical injury (above C5) compromises diaphragm; intubation often required
  • Spinal immobilization (rigid collar, log-roll precautions) until injury cleared
  • Maintain MAP 85-90 mm Hg for 7 days post traumatic SCI to support cord perfusion (vasopressors as needed)
  • Foley catheter for bladder management
  • Emergent neurosurgical or orthopedic spine consultation for decompression and stabilization
  • DVT prophylaxis (mechanical immediately; pharmacologic once hemorrhage excluded, typically within 72 h)
  • Corticosteroids (methylprednisolone) — NOT routinely recommended for traumatic SCI per current AANS/CNS guidance; risk of complications exceeds benefit

Central cord syndrome

  • Most common incomplete cervical SCI, often in older adults with cervical spondylosis after hyperextension
  • Upper extremity weakness > lower extremity, variable sensory loss, bladder dysfunction
  • Surgical decompression for instability or progressive deficit; otherwise conservative with reasonable prognosis for ambulation

Anterior cord syndrome

  • Loss of motor function + pain/temperature below lesion; preserved proprioception/vibration (posterior columns spared)
  • Often anterior spinal artery infarct (aortic surgery, dissection, atherosclerosis)
  • Poorest prognosis of incomplete syndromes

Brown-Séquard syndrome

  • Hemisection of cord — ipsilateral motor and dorsal column loss + contralateral pain/temp loss starting 1-2 levels below
  • Penetrating trauma, hemorrhage, tumor
  • Best prognosis among incomplete syndromes; most regain ambulation

Posterior cord syndrome

  • Loss of vibration/proprioception, sensory ataxia
  • Rare; consider B12 deficiency, tabes dorsalis, MS

Malignant epidural compression

  • Dexamethasone 10 mg IV bolus then 4 mg q6h
  • Urgent radiation oncology consultation
  • Surgical decompression for single-level disease, radioresistant tumor, instability, or need for tissue diagnosis (per Patchell trial)

Second-line / adjunct

  • Early multidisciplinary rehabilitation (PT, OT, SLP, rehabilitation medicine)
  • Bladder and bowel program
  • Pressure-injury prevention
  • Psychological support and peer support programs
  • Spasticity management: baclofen (oral or intrathecal), tizanidine, botulinum toxin

Complications

  • Neurogenic shock (hypotension + bradycardia) — distinguish from hemorrhagic shock
  • Spinal shock — transient flaccid areflexic state lasting hours-weeks
  • Autonomic dysreflexia — paroxysmal hypertension from noxious stimuli below T6 lesion; medical emergency: sit patient up, identify trigger (full bladder, fecal impaction), short-acting antihypertensive
  • Respiratory failure (high cervical injury), aspiration, pneumonia
  • Deep vein thrombosis and pulmonary embolism
  • Pressure injuries
  • Urinary tract infections, urolithiasis
  • Heterotopic ossification, contractures, spasticity
  • Chronic neuropathic pain
  • Depression and PTSD

PANCE pearls

  • Maintain MAP 85-90 mm Hg for 7 days after traumatic SCI to optimize cord perfusion and neurologic recovery.
  • Autonomic dysreflexia: think 'full bladder, full bowel, or pressure injury' — sit the patient up FIRST, then treat the trigger.
  • Methylprednisolone is no longer routinely recommended for acute traumatic SCI; check current AANS/CNS guidance and shared decision-making.
  • Beware the older adult who falls and complains of arm weakness with neck pain — central cord syndrome from cervical hyperextension.
  • Cancer patient with new back pain = MRI whole spine until proven otherwise; do not wait for neurologic deficit.

References

  • AANS/CNS 2013 — Walters BC et al. Guidelines for the management of acute cervical spine and spinal cord injuries: 2013 update. Neurosurgery 2013;72(Suppl 2):1-259.
  • ASIA 2019 — ASIA International Standards for Neurological Classification of Spinal Cord Injury (revised).
  • Patchell Trial — Patchell RA et al. Direct decompressive surgical resection in the treatment of spinal cord compression caused by metastatic cancer. Lancet 2005;366:643-648.
  • STASCIS — Fehlings MG et al. Early versus delayed decompression for traumatic cervical SCI. PLoS One 2012;7:e32037.

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