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). Acute non-traumatic compression commonly comes from epidural metastasis (lung, breast, prostate, multiple myeloma, lymphoma), epidural abscess, or hematoma; overall, degenerative cervical myelopathy is the most common cause of spinal cord dysfunction in adults.

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Question 1NeurologyMedium
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?
  • AEmergent surgical decompression
  • BIntravenous antihypertensive therapy
  • CTherapeutic anticoagulation
  • DHigh-dose intravenous corticosteroids
  • EMean arterial pressure augmentation
Reveal answer & full explanation
Correct answer: E — Mean arterial pressure augmentation
  • AEmergent surgical decompression
  • BIntravenous antihypertensive therapy
  • CTherapeutic anticoagulation
  • DHigh-dose intravenous corticosteroids
  • EMean arterial pressure augmentation✓

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

  • 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.
  • 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.
  • 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.
  • Intravenous antihypertensive therapy — aortic disease brings to mind aortic dissection, where blood pressure and heart rate are lowered, but this cord injury is ischemic and depends on perfusion pressure; lowering blood pressure would deepen the ischemia, and the fixed outflow obstruction of severe aortic stenosis makes hypotension especially poorly tolerated.

Additional high-yield points

  • Anterior cord syndrome carries the worst prognosis of the incomplete cord syndromes, underscoring the importance of optimizing perfusion early.
Question 2NeurologyMedium
A 68-year-old man is brought to the emergency department after tripping and striking his forehead on a coffee table. He reports immediate neck pain and bilateral hand weakness, saying he "can't grip anything." His past medical history includes cervical spondylosis. On examination, motor strength is 2/5 in the intrinsic hand muscles and wrist extensors but 4+/5 in the lower extremities, with a "cape-like" loss of pin-prick sensation over the shoulders. He has urinary retention. CT of the cervical spine shows no acute fracture, and MRI demonstrates cord signal change at C4-C5 within a stenotic canal. Which of the following is the most likely diagnosis?
  • APosterior cord syndrome
  • BCentral cord syndrome
  • CAnterior cord syndrome
  • DTransverse myelopathy
  • EBrown-Séquard syndrome
Reveal answer & full explanation
Correct answer: B — Central cord syndrome
  • APosterior cord syndrome
  • BCentral cord syndrome✓
  • CAnterior cord syndrome
  • DTransverse myelopathy
  • EBrown-Séquard syndrome

Why Central cord syndrome is correct

  • Central cord syndrome is the most common incomplete cervical cord injury, classically seen in an older adult with pre-existing cervical spondylosis after a hyperextension mechanism (a forward fall striking the face or forehead).
  • The hallmark pattern is upper-extremity weakness greater than lower-extremity weakness, often with a "cape" or dissociated sensory loss and early bladder dysfunction, because the centrally located gray matter and medial cord tracts are preferentially damaged.
  • MRI cord signal change within a stenotic canal at the cervical level confirms an intramedullary cord injury; management is MAP support, spine consultation, and decompression for instability or progressive deficit.

Why the others are wrong

  • Anterior cord syndrome - infarction or compression of the anterior two-thirds of the cord produces dense motor paralysis with loss of pain and temperature below the lesion while vibration and proprioception are spared, and it does not spare the legs; here the legs are 4+/5 while the hands are 2/5, the arm-greater-than-leg pattern of central gray injury.
  • Transverse myelopathy - an inflammatory myelopathy that evolves over hours to days with a clear sensory level, typically post-infectious or associated with MS or NMO; the acute traumatic hyperextension mechanism and central cord pattern here point to injury, not inflammation.
  • Brown-Séquard syndrome - cord hemisection, usually from penetrating or lateral compressive trauma, gives ipsilateral weakness and dorsal-column loss with contralateral pain and temperature loss below the lesion; this patient's hand weakness and cape-like pin-prick loss are symmetric and bilateral rather than crossed.
  • Posterior cord syndrome - the rarest incomplete cord syndrome, in which selective dorsal column injury causes loss of proprioception and vibration below the lesion with a sensory ataxic gait while strength and pain and temperature sensation are preserved; this patient's dominant findings are severe hand weakness and pin-prick loss, which travel in the corticospinal and spinothalamic tracts rather than the dorsal columns.

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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). ISNCSCI key muscles: C5 elbow flexors (biceps), C6 wrist extensors, C7 elbow extensors (triceps), C8 finger flexors, T1 small-finger abductors, L2 hip flexors, L3 knee extensors, L4 ankle dorsiflexors, L5 great-toe extensors, S1 ankle plantar flexors. Reflex levels: biceps C5-C6, triceps C7, patellar L4, Achilles S1.

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
  • Augment MAP to at least 75-80 mm Hg, without actively pushing above 90-95 mm Hg, for 3-7 days after traumatic SCI to support cord perfusion (vasopressors as needed); AO Spine/Praxis 2024 update of the older AANS/CNS 2013 target of 85-90 mm Hg for 7 days
  • 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
  • Ischemic (anterior spinal artery) infarct: support cord perfusion with MAP augmentation and strict avoidance of hypotension while treating the cause; steroids and surgical decompression are not indicated

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 triggered by noxious stimuli below the level of injury in lesions at or above T6; 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

  • After traumatic SCI, augment MAP to at least 75-80 mm Hg (upper limit 90-95 mm Hg) for 3-7 days and avoid any hypotension 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;60(CN Suppl 1):82-91.
  • 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.
  • AO Spine/Praxis 2024 — Kwon BK et al. A clinical practice guideline for the management of patients with acute spinal cord injury: recommendations on hemodynamic management. Global Spine J 2024;14(3 Suppl):187S-211S.

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