Transverse Myelitis

A focused approach to exam, imaging, differential, and acute management—an ideal companion topic to Guillain-Barré syndrome.

Topic: Spinal cord disorders Level: Intermediate Tags: myelitis, NMOSD, MOGAD, MS, cord compression

Overview

Transverse myelitis (TM) is an acute or subacute inflammatory injury of the spinal cord, producing motor, sensory, and autonomic dysfunction below the lesion. Patients typically develop back pain followed by bilateral limb symptoms over hours to days. TM may be idiopathic or secondary to conditions such as multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD, AQP4-IgG), myelin-oligodendrocyte glycoprotein–associated disease (MOGAD), infection, or systemic autoimmunity.

Clinician tip: Pronounce it “trans-VERSE my-uh-LIE-tis”. Early identification of a sensory level and sphincter symptoms fast-tracks imaging and treatment.

Core features

  • Back pain followed by rapidly evolving **bilateral** weakness and numbness below a **sensory level**.
  • Autonomic involvement: urinary retention, bowel dysfunction, sexual dysfunction.
  • Hyperreflexia and Babinski signs (upper motor neuron); early areflexia may appear at the level of the lesion.

Subtypes / related entities

Longitudinally extensive TM (LETM)

T2 lesion spanning ≥3 vertebral segments—consider NMOSD (AQP4-IgG), MOGAD, systemic autoimmune disease, or post-infectious causes.

Short-segment TM

1–2 segments—more typical of MS; look for brain MRI lesions disseminated in space/time.

Key differences at a glance

Feature Suggests Why it matters
Sensory level & UMN signs TM / spinal cord process Helps distinguish from peripheral causes like GBS (areflexia, no level).
LETM (≥3 vertebral segments) NMOSD/MOGAD, systemic autoimmunity Guides serologic testing and long-term immunotherapy.
Fever, focal spine tenderness Epidural abscess, osteomyelitis Urgent surgical/antimicrobial management.

Work-up snapshot

  • Neurologic exam: define sensory level, pyramidal signs, and sphincter function.
  • MRI spine with and without gadolinium: T2 hyperintensity; enhancement variable. Exclude compressive lesions first.
  • MRI brain: assess for MS or ADEM features.
  • CSF: pleocytosis and elevated protein common; oligoclonal bands suggest MS.
  • Serology: AQP4-IgG (NMOSD), MOG-IgG, autoimmune panel; targeted infectious testing as indicated (e.g., syphilis, HIV, Lyme).
Red flag: Suspected **cord compression** (severe focal pain, cancer, infection) is an emergency—obtain urgent MRI and neurosurgical/ID consultation.

Treatment snapshot

  • High-dose IV methylprednisolone (e.g., 1 g/day for 3–5 days) as first-line for inflammatory TM.
  • Plasma exchange for severe deficits or steroid-refractory cases; consider IVIG in select contexts.
  • Treat underlying cause (infectious, autoimmune), initiate bladder/bowel regimen, DVT prophylaxis, and early rehab.
Pearl: In LETM, send AQP4-IgG and MOG-IgG **before** immunotherapy if feasible; treatment should not be delayed for testing in severe cases.

References

  1. Wingerchuk DM et al. International consensus diagnostic criteria for NMOSD. Neurology. 2015.
  2. Jarius S, Paul F. MOG-IgG–associated disorders: diagnostic and treatment update. J Neuroinflammation. 2019.
  3. Transverse Myelitis Consortium Working Group. Proposed diagnostic criteria and evaluation. Neurology. 2002.

Educational discussion. Not a substitute for clinical judgment. Consider local protocols and individual factors.