Transverse Myelitis

FACTS

  • inflammatory condition of spinal cord
  • etiologies:
    • infectious
    • post-infectious (post-influenza)
    • traumatic
    • paraneoplastic
    • metabolic
    • autoimmune
 

HPI

universal ROS
  • ask about recent infection, trauma, cancer history, autoimmune history

PHYSICAL EXAM

universal neuro exam

IMAGING

Typical MRI findings in transverse myelitis
Feature
Description / Appearance
Notes / Key Points
T2-weighted signal
Hyperintense lesion within the spinal cord parenchyma
Most characteristic finding; represents edema and demyelination
T1-weighted signal
Often isointense or mildly hypointense
Severe or chronic lesions may show hypointensity from necrosis or cavitation
Gadolinium enhancement
Patchy, ring-like, or diffuse enhancement
Indicates active inflammation and breakdown of blood–spinal cord barrier
Cord swelling
Cord may appear expanded at the affected level
More common in acute phase
Lesion length
Usually ≥3 vertebral segments (“longitudinally extensive transverse myelitis” – LETM) in NMO, MOG-associated, or systemic autoimmune disease
<2 segments more typical of multiple sclerosis
Axial distribution
Central involvement (gray and white matter)
Helps distinguish from MS, which often affects peripheral white matter
Location
Often in thoracic cord, but may involve cervical or conus regions
Thoracic most common due to vascular watershed susceptibility

A/P

  • Lumbar puncture
  • Treat underlying cause
 

A. High-Dose IV Corticosteroids (First-Line)

  • Drug: Methylprednisolone
  • Dose: 1 g IV daily for 3–5 days
  • Mechanism: Suppresses inflammation and immune-mediated demyelination
  • Follow-up: May taper with oral prednisone (e.g., 60 mg daily with slow taper) depending on etiology and response
✅ Most patients are started on steroids immediately once infection and compressive causes are excluded (MRI and LP help rule out mimics).

B. Plasma Exchange (PLEX)

  • Indication:
    • Poor response to steroids after 3–5 days
    • Severe or rapidly progressive deficits
  • Typical regimen:
    • 5–7 exchanges over 10–14 days
  • Rationale: Removes pathogenic antibodies and immune complexes
  • Particularly helpful in:
    • Neuromyelitis optica (NMO) spectrum disorders
    • MOG-associated myelitis

C. IV Immunoglobulin (IVIG)

  • Alternative or adjunct when:
    • PLEX is contraindicated or unavailable
    • Post-infectious or para-infectious causes suspected
  • Dose: 0.4 g/kg/day for 5 days
 
Cause of TM
Examples
Specific Management
Autoimmune / NMO / MOG
NMO spectrum disorder, MOGAD, lupus, Sjögren’s
Immunosuppressants (rituximab, mycophenolate, azathioprine)
Infectious
HSV, VZV, syphilis, Lyme, HIV
Pathogen-specific antimicrobials (e.g., acyclovir, ceftriaxone)
Paraneoplastic
Associated with cancer
Treat underlying malignancy; consider immunotherapy
Idiopathic
None identified
Supportive + immunotherapy + rehab
 
 

MRI patterns broken down by etiology

Etiology
MRI Pattern
Comments
Idiopathic TM
Central T2 hyperintensity spanning 1–3 segments
Symmetric, no enhancement or mild patchy enhancement
NMO / MOG-associated
Longitudinally extensive (≥3 segments), often involving ≥2/3 of cord cross-section
May have ring or patchy enhancement; associated with optic neuritis
MS-related TM
Short segment (<2 segments), peripheral or dorsal-lateral
Often associated with brain lesions typical for MS
Infectious / post-infectious
Variable enhancement and edema
Often symmetric, diffuse involvement
Ischemic myelopathy
“Pencil-like” anterior cord hyperintensity, sometimes with “owl’s eyes” on axial
Usually non-enhancing, abrupt onset