A patient with a T11 compression fracture now presents with acute motor weakness, sensory loss at a distinct level, and bladder/bowel dysfunction—how can I differentiate transverse myelitis from traumatic injury, and what MRI, cerebrospinal fluid studies, and treatment (high‑dose intravenous methylprednisolone and plasma exchange) are indicated?

Differentiating Transverse Myelitis from Traumatic Spinal Cord Injury in T11 Compression Fracture

In a patient with T11 compression fracture presenting with acute motor weakness, sensory level, and bladder/bowel dysfunction, obtain urgent MRI of the entire spine with thin axial cuts and initiate high-dose intravenous methylprednisolone (1g daily for 3-5 days) immediately while awaiting diagnostic confirmation, as delay beyond 2 weeks significantly worsens neurological outcomes. 1, 2

Clinical Differentiation

Key Distinguishing Features

Hyperreflexia (increased deep tendon reflexes) strongly suggests transverse myelitis rather than acute traumatic injury, as this finding indicates an upper motor neuron inflammatory process rather than spinal shock from trauma 2. In contrast, acute traumatic spinal cord injury typically presents with areflexia or hyporeflexia during the initial spinal shock phase 2.

The temporal profile matters critically:

• Transverse myelitis progresses over hours to days, with most cases reaching maximal severity within 10 days of onset 3
• Traumatic injury causes immediate deficits at the time of fracture, though delayed deterioration can occur with epidural hematoma or progressive compression 4

Diagnostic Workup

Immediate MRI Protocol

MRI of the entire spine (cervical, thoracic, and lumbar) with thin axial cuts through the T11 region is essential, not just imaging of the fracture site 4, 1, 2. This comprehensive approach is critical because:

• T2-weighted sequences will show hyperintense signal within the spinal cord parenchyma in transverse myelitis, extending beyond the fracture site 1, 2, 3
• Longitudinally extensive lesions affecting ≥3 vertebral segments suggest neuromyelitis optica spectrum disorder (NMOSD) rather than idiopathic transverse myelitis 1, 2
• Traumatic injury shows cord compression, epidural hematoma, or contusion localized to the fracture level without intrinsic T2 hyperintensity extending multiple segments 4
• Conus medullaris involvement suggests MOG antibody-associated disease (MOGAD) 2

Cerebrospinal Fluid Analysis

Perform lumbar puncture urgently to check cell count, protein, glucose, oligoclonal bands, viral PCRs, and onconeural antibodies 1, 2. CSF findings help distinguish etiologies:

• Mild-to-moderate pleocytosis (50-70% of cases) with elevated protein supports inflammatory transverse myelitis 4
• Intensely inflammatory CSF resembling bacterial meningitis necessitates antimicrobial therapy while continuing corticosteroids 4
• Normal or minimally abnormal CSF does not exclude transverse myelitis but makes traumatic etiology more likely 4

Blood Testing

Obtain aquaporin-4 IgG (serum, not CSF), MOG antibodies (cell-based assay), B12, HIV, RPR, ANA, Ro/La, and TSH 1, 2. These tests differentiate:

• Positive aquaporin-4 IgG confirms NMOSD, which requires more aggressive immunosuppression 1, 2
• Positive MOG antibodies suggest MOGAD, characterized by steroid-dependent recurrent myelitis 2
• HIV and syphilis (RPR) screening is mandatory as infectious causes require specific antimicrobial therapy 1, 2

Brain MRI

Obtain brain MRI with and without contrast to evaluate for demyelinating lesions, as this distinguishes multiple sclerosis from isolated transverse myelitis and helps exclude other CNS pathology 4, 2.

Treatment Algorithm

Immediate Management (Within Hours)

Initiate high-dose intravenous methylprednisolone 1g daily for 3-5 days immediately, even before diagnostic confirmation, as delays beyond 2 weeks are associated with severe neurological deficits 4, 1. This aggressive early approach is justified because:

• Neurological response parallels MRI improvement within days to 3 weeks when treatment is prompt 4
• The combination of methylprednisolone and cyclophosphamide is effective if used within the first few hours 4

Moderate to Severe Cases

For patients with significant motor weakness or sensory changes, combine corticosteroids with IVIG 2g/kg over 5 days 1. This dual therapy approach provides broader immunosuppression for severe inflammatory disease.

Refractory Cases (Second-Line)

Plasma exchange therapy should be initiated for patients not responding adequately to corticosteroids and IVIG within 3-5 days 4, 1. Plasma exchange has demonstrated efficacy in severe cases, particularly when started early 4.

Consider rituximab for cases with positive autoimmune antibodies or inadequate response to standard therapies 1.

Maintenance Therapy

After acute treatment, initiate maintenance immunosuppressive therapy (such as azathioprine) to prevent relapses, which occur in 50-60% of cases during corticosteroid dose reduction 4, 1. This is a critical pitfall—failure to provide maintenance therapy leads to high relapse rates.

Special Considerations

Antiphospholipid Antibody-Positive Cases

Add anticoagulation therapy for patients with positive antiphospholipid antibodies, as thrombotic mechanisms contribute to cord injury in these cases 4, 1.

Infectious Etiology

If infectious myelitis is identified (e.g., schistosomiasis), administer appropriate antimicrobial therapy alongside corticosteroids 1. However, bacterial or HSV infection requires antimicrobial/antiviral therapy as primary treatment 4.

Prognostic Factors

Poor outcomes are associated with:

• Extensive spinal cord MRI lesions (≥3 vertebral segments) 4, 1
• Reduced muscle strength or sphincter dysfunction at presentation 4, 1
• Delay >2 weeks in initiating therapy 4, 1

These factors should prompt more aggressive initial treatment and closer monitoring.

Critical Pitfalls to Avoid

Do not assume neurological deficits are solely traumatic in a patient with compression fracture—the presence of hyperreflexia, progression over days, or MRI findings of intrinsic cord signal abnormality extending beyond the fracture site mandate evaluation and treatment for transverse myelitis 2, 3.

Do not delay corticosteroid therapy while awaiting complete diagnostic workup—early treatment (within hours) is associated with significantly better outcomes 4, 1.

Do not discontinue immunosuppression after acute treatment without maintenance therapy—relapse rates of 50-60% during steroid taper necessitate long-term immunosuppression 4, 1.