Transverse myelitis

Transverse myelitis (TM) is an acute or subacute inflammation of the spinal cord, causing demyelination and neuronal injury across one or more spinal segments. It leads to bilateral motor, sensory, and autonomic dysfunction below the level of the lesion.

• inflammation within the spinal cord results in demyelination and axonal damage
• disruption of ascending sensory and descending motor pathways leads to neurological deficits below the lesion
• involvement of autonomic tracts causes bladder, bowel, and sexual dysfunction
• the lesion is typically central and may extend over one or more vertebral segments
• MRI often shows longitudinally extensive lesions in neuromyelitis optica and shorter, patchy lesions in multiple sclerosis

• autoimmune or inflammatory: multiple sclerosis, neuromyelitis optica spectrum disorder, systemic lupus erythematosus, Sjögren’s syndrome, sarcoidosis
• post-infectious or para-infectious: immune-mediated inflammation following viral or bacterial infection (varicella-zoster, herpes simplex, cytomegalovirus, Epstein–Barr, influenza, syphilis, Lyme disease)
• infectious: direct invasion by viruses (e.g. HIV) or bacteria (e.g. tuberculosis, mycoplasma)
• paraneoplastic: associated with malignancies such as small cell lung carcinoma
• vascular: spinal cord ischaemia or infarction mimicking TM
• drug-induced or toxin-related: rare reactions to TNF-α inhibitors, immune checkpoint inhibitors, or certain antimicrobials
• idiopathic: no identifiable cause in around one-third of cases

• onset is typically acute or subacute (hours to days)
• bilateral motor weakness below the level of the lesion
• sensory loss with a distinct sensory level on examination
• autonomic dysfunction
• urinary retention or incontinence
• constipation or faecal incontinence
• sexual dysfunction
• back pain or radicular pain may precede neurological deficits

• MRI of the spine with contrast
• shows focal or longitudinal spinal cord inflammation
• helps exclude compressive causes
• MRI brain
• assesses for demyelinating lesions suggestive of multiple sclerosis
• lumbar puncture
• may show raised protein, mild lymphocytic pleocytosis, or oligoclonal bands (in MS)
• blood tests
• autoimmune screen (ANA, ENA, anti–aquaporin-4, anti–MOG antibodies)
• infection screen: viral serology, syphilis, Lyme
• consider CT chest or PET if sarcoidosis or malignancy suspected

• treat underlying cause if identified (e.g. antibiotics for infection)
• high-dose IV corticosteroids
• e.g. methylprednisolone 1 g daily for 3–5 days
• dexamethasone 16–20 mg daily IV may be used as an alternative if methylprednisolone is unavailable
• plasma exchange if poor response to steroids or in NMOSD
• long-term immunosuppression (azathioprine, mycophenolate, rituximab) in recurrent or autoimmune cases
• supportive therapy
• physiotherapy and rehabilitation
• bladder and bowel management
• venous thromboembolism prophylaxis

• recovery begins within 2–12 weeks; most improve partially, but some are left with residual weakness or spasticity
• poor prognostic factors include rapid onset, complete paraplegia at presentation, and extensive MRI lesions