What neurological deficits may occur with severe wedge fractures of T10 and T11, spinal cord compression at T11, and edema involving the T10-11 intervertebral disc?

Neurological Deficits Associated with T10-T11 Wedge Fractures and Spinal Cord Compression

Patients with severe wedge fractures of T10 and T11 with spinal cord compression at T11 due to retropulsed vertebral body will likely present with significant lower extremity weakness, sensory disturbances, and potential bowel/bladder dysfunction requiring immediate surgical intervention.

Expected Neurological Deficits

Thoracic spinal cord compression at the T10-T11 level typically produces a constellation of neurological deficits due to the anatomical location and function of neural structures at this level:

Motor Deficits

• Moderate to severe lower extremity weakness affecting both legs
• Increased patellar tendon reflexes (hyperreflexia) due to upper motor neuron involvement 1
• Spasticity in the lower extremities
• Possible gait disturbance or inability to walk depending on severity

Sensory Deficits

• Sensory disturbances affecting the entire lower extremities 1
• Loss of sensation below the level of injury (approximately at the umbilicus)
• Potential loss of proprioception and vibration sense
• Possible dysesthesias or paresthesias in affected dermatomes

Autonomic Dysfunction

• Bowel and bladder dysfunction (incontinence or retention)
• Sexual dysfunction
• Potential orthostatic hypotension
• Thermoregulatory disturbances below the level of injury

Pathophysiological Basis

The neurological deficits observed are directly related to the pathophysiology of spinal cord compression:

1. Direct mechanical compression: The retropulsed vertebral body fragment directly compresses neural elements, causing immediate neurological deficits 2

2. Secondary injury mechanisms: Edema involving the T10-11 intervertebral disc can exacerbate compression and cause progressive neurological deterioration 3

3. Vascular compromise: Compression can impair blood supply to the spinal cord, leading to ischemia and worsening of neurological function

Clinical Presentation Pattern

The pattern of deficits is consistent with an upper motor neuron lesion at the thoracolumbar junction:

• T10-T11 disc herniations typically present with moderate lower extremity weakness, increased patellar reflexes, and sensory disturbance of the entire lower extremities 1
• The severity of neurological deficits correlates with the degree of canal compromise, with 50% or greater decrease in mid-sagittal neural canal diameter carrying significant risk of neurological involvement 2

Management Implications

The presence of these neurological deficits has important management implications:

1. Immediate surgical intervention: Surgery is the standard of care for vertebral fractures complicated by spinal cord compression and neurological deficits 3

2. Corticosteroid administration: High-dose dexamethasone (16 mg/day) should be administered promptly when spinal cord compression is suspected, even before radiographic confirmation 3

3. Timing of intervention: Early surgical decompression (within 48 hours) is associated with better neurological outcomes 3

4. Surgical approach: Decompressive surgery with tumor excision and stabilization can improve neurological status from non-ambulatory to ambulatory 3

Prognostic Factors

Several factors influence the prognosis for neurological recovery:

• Severity and duration of neurological deficits before treatment
• Extent of spinal cord compression on imaging
• Timing of surgical intervention
• Patient age and comorbidities

Common Pitfalls to Avoid

1. Delayed diagnosis: Progressive neurological deficits can develop early after injury, particularly with burst fractures at the thoracolumbar junction 2

2. Inadequate imaging: MRI of the entire spine is essential to fully evaluate the extent of injury and to exclude additional levels of compression 3

3. Insufficient decompression: Failure to adequately decompress the spinal cord can result in persistent or progressive neurological deficits

4. Overlooking instability: Addressing both the neural compression and spinal instability is crucial for optimal outcomes 4

The neurological presentation of thoracolumbar junction injuries is complex due to the transition from spinal cord to cauda equina at this level. Prompt recognition and appropriate management are essential to maximize neurological recovery and prevent further deterioration.