Will transverse myelitis patients develop flaccid or spastic paralysis and changes in reflexes?

Transverse Myelitis Patients Develop Spastic Paralysis with Increased Deep Tendon Reflexes

Patients with transverse myelitis typically develop spastic paralysis with increased deep tendon reflexes rather than flaccid paralysis, as the condition primarily affects the spinal cord causing upper motor neuron damage. 1

Clinical Presentation of Transverse Myelitis

• Transverse myelitis presents with acute or subacute bilateral weakness or sensory changes, often accompanied by increased deep tendon reflexes due to the upper motor neuron involvement 1
• The condition involves an immune-mediated process causing neural injury to the spinal cord, resulting in varying degrees of weakness, sensory alterations, and autonomic dysfunction 2
• Symptoms typically develop rapidly with progressive paralysis of the extremities, which is characteristic of spastic rather than flaccid presentation 3

Pathophysiology and Neurological Findings

• Transverse myelitis affects the spinal cord gray matter, leading to upper motor neuron damage above the level of the lesion 1
• This upper motor neuron involvement results in spastic paralysis with hyperreflexia (increased reflexes) rather than the flaccid paralysis and hyporeflexia seen in lower motor neuron disorders 1
• MRI findings typically show T2-weighted hyperintense lesions in the spinal cord that may appear wedge-shaped on axial views and cigar-shaped on sagittal views 1

Differential Considerations

• It's important to distinguish transverse myelitis from conditions that cause flaccid paralysis:
  • Guillain-Barré syndrome (GBS) presents with flaccid paralysis and reduced/absent reflexes due to peripheral nerve involvement 1
  • Acute flaccid myelitis primarily affects anterior horn cells causing flaccid paralysis, and is often associated with enterovirus infections (particularly D68) 4
  • Poliomyelitis and other enterovirus infections can cause an encephalitis with acute flaccid paralysis 1

Diagnostic Approach

• Neurologic consultation should be obtained promptly 1
• MRI of the spine with thin axial cuts through the region of suspected abnormality is essential 1
• Lumbar puncture should be performed to check cell count, protein, glucose, oligoclonal bands, viral PCRs, and onconeural antibodies 1
• Blood tests should include B12, HIV, RPR, ANA, Ro/La, TSH, and aquaporin-4 IgG to rule out other causes 1
• Evaluation for urinary retention and constipation is important as these are common autonomic manifestations 1

Clinical Course and Management

• Transverse myelitis has a variable prognosis, with some patients recovering completely while others develop permanent disabilities 3
• First-line treatment typically includes high-dose intravenous corticosteroids (methylprednisolone 1g/day for 3-5 days) 1
• For moderate to severe cases, additional therapies such as intravenous immunoglobulin (IVIG) should be strongly considered 1
• In refractory cases, plasma exchange therapy or rituximab may be beneficial 1
• Early aggressive treatment is crucial to improve outcomes and reduce long-term disability 5

Important Clinical Pearls

• The presence of increased deep tendon reflexes is a key distinguishing feature of transverse myelitis compared to conditions with flaccid paralysis 1
• Longitudinally extensive transverse myelitis (affecting ≥3 vertebral segments) should raise suspicion for neuromyelitis optica spectrum disorder (NMOSD) 1
• Persistent flaccid paralysis and electrophysiological evidence of axonal loss generally portend a poorer prognosis 3
• Transverse myelitis may occur as an isolated idiopathic entity or as part of a multifocal CNS disease (e.g., MS) or multisystemic disease (e.g., systemic lupus erythematosus) 2