At a glance
What it is
Transverse myelitis (TM) is an inflammatory myelopathy in which focal inflammation at one or more spinal cord levels disrupts the sensory, motor, and autonomic tracts passing through. The term 'transverse' implies dysfunction across the cord at a given level — though anatomically complete transverse disruption is rare; partial cord involvement is more common. TM can be idiopathic (cause unknown) or associated with autoimmune disease (multiple sclerosis, neuromyelitis optica spectrum disorder/NMOSD, SLE, Sjögren's, sarcoidosis) or infection. It affects all ages and both sexes. In younger patients, TM may be the first presentation of MS or NMOSD.
Symptoms
Symptoms develop over hours to days. Limb weakness — from mild heaviness to complete paralysis — below the level of cord inflammation; distribution depends on the cord level affected (legs only for thoracic TM; arms and legs for cervical TM). Sensory disturbance: pain (sudden back or radicular pain at the lesion level), then numbness, tingling, and a feeling of tight banding around the chest or abdomen. Bladder and bowel dysfunction: urinary urgency, retention, or incontinence; constipation. About one-third recover fully; one-third have moderate disability; one-third have severe permanent disability. Recovery occurs mainly in the first 3 months and is strongly influenced by the underlying cause.
Approach
Urgent MRI of the full neuraxis (brain + spine) is essential to confirm myelitis, determine the extent of cord signal change, and identify any brain lesions suggesting MS or NMOSD. Blood tests include NMO-IgG (aquaporin-4 antibody), MOG-IgG, ANA, anti-dsDNA, ACE (sarcoidosis), and infectious serology. CSF analysis looks for inflammation and infection. Acute treatment: high-dose IV methylprednisolone (1 g/day × 5 days). Plasma exchange (PLEX) for steroid-non-responders. Long-term: disease-modifying therapy for MS or NMOSD-related TM to prevent recurrence; physical and occupational rehabilitation; spasticity management; bladder management; neuromodulation for chronic pain.
What transverse myelitis is
The spinal cord carries all signals between the brain and the body. When a segment becomes inflamed — with breakdown of the myelin sheath (demyelination) and, in severe cases, axonal damage — the passage of signals through that level is disrupted. Everything below the lesion is affected to a variable degree.
**Causes and classification**
*Idiopathic TM* — no underlying cause is identified even after complete work-up. This is, paradoxically, a diagnosis of exclusion. Some idiopathic cases are later reclassified when a cause emerges.
*Multiple sclerosis (MS)* — TM in MS typically causes a short (< 2 vertebral segments), asymmetric, partial cord lesion. MRI of the brain shows periventricular white matter lesions. CSF may show oligoclonal bands. TM as the first MS attack (clinically isolated syndrome) requires disease-modifying therapy to prevent further relapses.
*Neuromyelitis optica spectrum disorder (NMOSD)* — TM in NMOSD is typically longitudinally extensive (≥ 3 vertebral segments), severe, and centred on the grey matter. Serum NMO-IgG (aquaporin-4 antibody) is positive in ~70% of NMOSD patients; MOG-IgG is positive in MOG-antibody disease. NMOSD requires long-term immunosuppression (rituximab, eculizumab, inebilizumab, or azathioprine) to prevent recurrent attacks.
*Post-infectious TM* — an immune-mediated reaction to a preceding viral or bacterial infection, occurring days to weeks after the illness. Viruses (herpes, cytomegalovirus, EBV, enterovirus, influenza, COVID-19) and bacteria (Lyme disease, syphilis, tuberculosis) are implicated.
*Systemic autoimmune diseases* — SLE, Sjögren's syndrome, sarcoidosis, and mixed connective tissue disease can cause TM as part of CNS involvement.
**Recovery and prognosis**
Recovery from TM begins within weeks of the acute phase. Most improvement occurs within 3–6 months; further slow recovery can occur over 1–2 years. Poor prognostic signs: complete cord lesion, rapid progression to paralysis, absence of pain at onset, NMOSD aetiology, absence of early steroid response.
**Chronic management**
Chronic sequelae — spasticity, neuropathic pain, bladder and bowel dysfunction, fatigue, depression — require a multidisciplinary approach. Spasticity responds to physiotherapy, baclofen, and Botox®. Neuropathic pain is managed with anticonvulsants (pregabalin, gabapentin) or antidepressants (duloxetine). Bladder dysfunction requires urological review; intermittent self-catheterisation may be needed. Neuromodulation (rTMS, tDCS, SCS, intrathecal baclofen pump) has a role in refractory spasticity and chronic pain.
Treatment options at Alimran Medical Center
Neuromodulation
Injection therapies
- Botox® injections
- Prolotherapy
- Ozone injection
- Trigger point injections
- Epidural steroid injections
Advanced therapies
Physiotherapy & rehabilitation
- Electrical stimulation
- Short and long wave therapy
- Laser therapy
- Ultrasound therapy
- Spasticity rehabilitation and bladder retraining
- SpineMED® system
- Sigma
Book a consultation
The secretary schedules first appointments during clinic hours; please have prior imaging, operative notes and a current medication list available at the time of the call.
This page provides general information about transverse myelitis and is not a substitute for individual medical assessment. If your symptoms are severe or worsening, contact a clinician promptly.