Transverse Myelitis (TM)

Definition

• ROSEN's Emergency Medicine, p. 1508

Causes / Etiology

1. Post-infectious / Para-infectious (most common, ~30%)

• Follows viral infection (e.g., herpes simplex, varicella-zoster, cytomegalovirus, Epstein-Barr virus, HIV, West Nile virus, COVID-19)
• Bacterial: mycoplasma, Lyme disease (rare)
• Post-vaccination (rare)

2. Autoimmune / Demyelinating CNS Diseases

• Multiple sclerosis (MS) - partial/asymmetric TM is a common presenting feature
• Neuromyelitis Optica Spectrum Disorder (NMOSD) - associated with anti-aquaporin-4 (anti-AQP4) antibodies; causes longitudinally extensive TM (LETM) spanning 3+ vertebral levels
• MOG Antibody Disease (MOGAD) - anti-myelin oligodendrocyte glycoprotein antibodies
• Acute disseminated encephalomyelitis (ADEM)

3. Systemic Autoimmune / Connective Tissue Diseases

• Systemic lupus erythematosus (SLE)
• Sjogren syndrome
• Antiphospholipid antibody syndrome
• Vasculitis, sarcoidosis
• Mixed connective tissue disease, rheumatoid arthritis, scleroderma, Behcet disease
• Goldman-Cecil Medicine, p. 3995

4. Vascular

• Spinal cord ischemia / infarction (dural venous fistula, antiphospholipid syndrome)

5. Paraneoplastic

• Associated with occult malignancy

Clinical Features

1. Motor Deficits

• Bilateral weakness (paraparesis or paraplegia) - may be asymmetrical
• Progresses to spasticity with upper motor neuron signs: hypertonia, hyperreflexia, clonus, positive Babinski response
• In early/acute phase: spinal shock may produce flaccid paralysis with hyporeflexia

2. Sensory Deficits

• Clearly defined sensory level on the trunk - hallmark finding
• Ascending paresthesias (numbness, tingling, burning)
• Loss of deep sensation (proprioception, vibration) in feet
• All modalities below the lesion affected in complete TM

3. Autonomic / Sphincter Dysfunction

• Urinary retention or incontinence (bladder is involved in nearly all patients)
• Fecal retention or incontinence
• Sexual dysfunction
• Autonomic instability in high cervical/thoracic lesions: hyper- or hypotension, tachy- or bradycardia

4. Pain

• Neck or back pain is common at onset
• Low-grade fever may be present (raises concern for septic epidural abscess as differential)

Complete vs. Partial TM

• Complete (LETM): total loss of all motor, sensory, and sphincter function below the level - hallmark of NMOSD
• Partial TM: incomplete, asymmetric deficits - more associated with MS

Gold Standard Diagnosis

Primary Investigation: MRI Spine with Gadolinium

• T2-weighted images: focal hyperintense (bright) signal within the spinal cord - present in 50-90% of adults
• T1-weighted images: iso- or mildly hypointense signal; cord swelling over several segments
• Gadolinium enhancement: indicates active inflammation (enhancement occurs within 7 days of onset)
• LETM: T2 signal spanning 3 or more vertebral levels - strongly suggests NMOSD

MRI findings in demyelinating disease. Lower right shows multiple discrete hyperintense spinal cord plaques, with acute cord expansion at C3. - Adams and Victor's Principles of Neurology

Supporting Investigations

Diagnostic Criteria (Transverse Myelitis Consortium Working Group 2002)

1. Neurologic symptoms attributable solely to the spinal cord
2. Bilateral signs/symptoms (may be asymmetric)
3. Clearly defined sensory level
4. MRI exclusion of cord compression
5. Inflammation in cord: CSF pleocytosis, elevated IgG index, OR gadolinium enhancement (within 7 days)
6. Progressive worsening peaking between 4 hours and 21 days after onset
7. No other etiology (infection, neoplasm, trauma, vascular, nutritional deficiency)

Physiotherapy Treatment

Acute Phase - Immediate Goals

1. Positioning and Skin Care

• Correct limb positioning to prevent contractures and pressure injuries
• Regular 2-hourly turning schedule
• Use of pressure-relieving mattresses/cushions
• Splinting of ankles/wrists in neutral to prevent deformity

2. Passive Range of Motion (PROM) Exercises

• All paralyzed limb joints taken through full range of motion daily
• Maintains joint mobility and prevents contractures
• Prevents deep vein thrombosis (DVT) by promoting venous return
• Focus on: hip, knee, ankle (dorsiflexion), shoulder, elbow, wrist

3. Respiratory Physiotherapy (especially cervical/high thoracic lesions)

• Intercostal and diaphragmatic breathing exercises
• Assisted coughing techniques (manual costal compression)
• Incentive spirometry
• Postural drainage and percussion if secretions present
• Aim: prevent pneumonia and respiratory failure

4. Edema Management

• Elevation of limbs
• Compression stockings/bandaging to prevent dependent edema
• Early gentle massage

5. Spasticity Management

• Stretching programs (sustained slow stretching)
• Neutral positioning
• Splinting
• Preparation for pharmacological management (baclofen, tizanidine - to be coordinated with medical team)

6. Neuromuscular Stimulation

• Electrical stimulation (NMES/FES) to maintain muscle bulk and facilitate motor return
• Sensory stimulation to affected areas

7. Active Exercises (when voluntary movement present)

• Active-assisted to active range of motion exercises as tolerated
• Strengthening of partially preserved muscle groups
• Neuromuscular re-education

8. Bladder and Bowel Management

• Bladder rehabilitation: timed voiding, pelvic floor exercises if possible
• Intermittent catheterization program coordination with nursing

9. Early Mobilization (when hemodynamically stable)

• Head-of-bed elevation to prevent orthostatic hypotension
• Tilt table standing (graded)
• Transfer training (bed to chair)
• Wheelchair mobility if applicable

10. Psychological Support

• Reassurance and education of patient and family
• Goal setting and explanation of recovery trajectory

Summary Table: Acute Phase Physiotherapy

Medical Treatment (for context)

• First-line: IV methylprednisolone 1000 mg/day for 3-5 days
• Refractory cases: Plasma exchange (IVIG or plasmapheresis), cyclophosphamide
• NMOSD: Long-term immunosuppression (azathioprine, rituximab, satralizumab, eculizumab)

Prognosis

• ~30% good recovery, 25% fair, 30% poor, 15% mortality in severe cases
• Recovery begins within 1-3 months; maximal improvement by 3-6 months
• Poor prognostic factors: rapid onset to nadir (<24 hours), complete cord involvement, NMOSD