What are the differential diagnoses for acute or sub‑acute paraplegia?

Differential Diagnosis of Acute or Subacute Paraplegia

The differential diagnosis for acute or subacute paraplegia must be systematically approached by first distinguishing between compressive and non-compressive etiologies, as this fundamentally determines both urgency and management strategy 1.

Primary Categorization Framework

The most critical initial step is determining whether spinal cord compression is present, as this represents a surgical emergency. Once compression is excluded, the differential expands to include intrinsic cord pathologies.

Compressive Causes (Extrinsic)

These require immediate identification as they often necessitate urgent surgical intervention:

• Traumatic: Vertebral fractures, dislocations, epidural hematoma
• Degenerative: Severe disc herniation (particularly cervical), spondylotic myelopathy with acute decompensation
• Neoplastic: Epidural metastases, primary spinal tumors causing cord compression
• Infectious: Epidural abscess, vertebral osteomyelitis with cord compression
• Vascular: Epidural hematoma (spontaneous or anticoagulation-related)
• Post-surgical: Early postoperative hematoma 1

Non-Compressive Causes (Intrinsic)

Once extrinsic compression is excluded, consider these intrinsic cord pathologies 1:

Vascular Etiologies

• Spinal cord infarction: Most commonly from anterior spinal artery occlusion, vertebral artery dissection, or aortic pathology (including acute aortic occlusion which can present with flaccid paraplegia even with palpable distal pulses initially) 1, 2
• Spinal dural arteriovenous fistula/malformation: Can present acutely with hematomyelia 1

Inflammatory/Demyelinating Diseases

• Multiple Sclerosis (MS): Affects 80-90% of MS patients, most commonly cervical cord 1
• Neuromyelitis Optica (NMO): Characterized by longitudinally extensive transverse myelitis and optic neuritis 1
• Acute Disseminated Encephalomyelitis (ADEM): Spinal involvement in ~25% of cases 1
• Systemic inflammatory conditions: Systemic lupus erythematosus, Sjögren syndrome, Behçet disease, sarcoidosis 1

Infectious Etiologies

• Viral myelitis: Including human T-cell lymphotropic virus (HTLV), HIV vacuolar myelopathy
• Bacterial: Tuberculosis, tertiary syphilis
• Parasitic: Schistosomiasis 1

Metabolic/Toxic Causes

• Subacute combined degeneration: Vitamin B12 (cobalamin) deficiency, copper deficiency
• Nitrous oxide toxicity 1

Neoplastic (Intramedullary)

• Primary spinal cord tumors: Astrocytomas, ependymomas
• Metastatic intramedullary lesions (rare) 1

Autoimmune

• Paraneoplastic myelopathy
• Antibody-mediated myelitis (including MOG, aquaporin-4 antibodies) 1, 3

Rare Structural Causes

• Hirayama disease (cervical flexion myelopathy)
• Dorsal arachnoid webs
• Ventral cord herniation 1

Critical Diagnostic Pitfalls

Do not assume spinal cord pathology is the only cause of paraplegia. Rare but important mimics include:

• Bilateral precentral gyri cerebral contusions: Can cause pure motor paraplegia without sensory level, easily missed on acute CT 4
• Acute aortic occlusion: Can present as flaccid paraplegia with severe back pain, even with initially palpable distal pulses 2
• Cervical disc herniation: Can cause acute paraplegia in patients with pre-existing canal stenosis, even without antecedent trauma 5

Imaging Strategy

MRI of the spine with and without IV contrast is the definitive initial imaging modality 1. Key technical considerations:

• Include diffusion-weighted imaging (DWI) when spinal cord ischemia is suspected, as it shows signal changes earlier than T2-weighted sequences 1
• Contrast enhancement is essential for initial evaluation to distinguish inflammatory/infectious from ischemic etiologies and to identify tumors 1
• Image the entire spine when demyelinating disease is suspected, as MS most commonly affects the cervical cord 1

CT myelography serves as an alternative when MRI is contraindicated, though it provides inferior soft tissue detail 1.

Time-Critical Considerations

The distinction between acute (maximum deficit within 21 days) versus subacute presentation helps narrow the differential 3. Hyperacute presentations (hours) favor vascular or compressive etiologies, while progression over days to weeks suggests inflammatory, infectious, or metabolic causes.

Radiation-induced myelopathy should be considered in patients with prior radiation therapy, as it anatomically localizes to the previous radiation port 1.