Introduction

Brown-Séquard syndrome (also known as Brown-Séquard’s hemiplegia or paralysis,hemiparaplegic syndrome, hemiplegia et hemiparaplegia spinalis, or spinal hemiparaplegia) is caused by damage to one half of the spinal cord, resulting in paralysis and loss of proprioception on the same (or ipsilateral) side as the injury or lesion, and loss of pain and temperature sensation on the opposite (or contralateral) side as the lesion.

• Unilateral involvement of the dorsal column, corticospinal tract, and spinothalamic tract

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History

The disease is named after physiologist Charles-Édouard Brown-Séquard, who first described the condition in 1850.

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Aetiology

Causes of spinal cord hemisection:

• Penetrating trauma from a stab, bullet
• Fracture-dislocation
• Spinal cord tumour
• Disc herniation
• Syringomyelia
• Hematomyelia

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Pathophysiology

The hemisection of the cord results in a lesion of each of the 3 main neural systems:

• Descending corticospinal tract (UMN lesion)
• Ascending dorsal columns (One or both):
  • Fasciculus gracilis
  • Fasciculus cuneatus 
• Spinothalamic tracts

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Clinical features

Ipsilateral loss of motor function and proprioception (same side of lesion):

• Hemisection causes damage to the ipsilateral descending motor pathways and ascending proprioceptive pathways which cross in the brainstem
• The corticospinal tract is disrupted, which carries motor function
• The dorsal column is disrupted, which carries proprioception (position sense and vibratory sense)

Contralateral loss of pain and temperature sensation:

• Hemisection causes damage to the contralateral sensory pathways for pain and temperature which cross at their spinal root levels
• Pain/temperature loss occurs below the level of the lesion
• The spinothalamic tract is disrupted, which carries pain and temperature sensation from the contralateral side of the body

Pure Brown-Séquard syndrome is associated with the following:

• Interruption of the lateral corticospinal tracts:
  • Ipsilateral spastic paralysis below the level of the lesion
  • Babinski sign ipsilateral to lesion
  • Abnormal reflexes and Babinski sign may not be present in acute injury.
• Interruption of posterior white column:
  • Ipsilateral loss of tactile discrimination, vibratory, and position sensation below the level of the lesion
• Interruption of lateral spinothalamic tracts:
  • Contralateral loss of pain and temperature sensation.
  • 2–3 segments below the level of the lesion

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Diagnosis

Imaging

MRI:

Differential diagnosis

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Management

Supportive management

• Rehabilitation:
  • Physical & occupational therapy
• Swelling/inflammation:
  • Corticosteroids

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Summary