Brown-Séquard syndrome

Brown-Séquard syndrome (also known as Brown-Séquard's hemiplegia, Brown-Séquard's paralysis, hemiparaplegic syndrome, hemiplegia et hemiparaplegia spinalis, or spinal hemiparaplegia) is a neurological condition caused by damage to one half of the spinal cord. The condition presents clinically with spastic paralysis and loss of fine touch perception, vibratory sensation and proprioception just below the lesion on the same side of the body as the lesion, but with loss of crude touch, pain an temperature sensation and on the opposite side and beginning somewhat lower than the lesion. At the level of the lesion, on the same side of the lesion, there is meanwhile a region of flaccid paralysis and complete loss of all sensation.

Brown-Séquard syndrome
Other names	Brown-Séquard's paralysis
Specialty	Neurology

Because injury to a whole half but only one half of the spinal cord only rarely occurs under real-life circumstances, the condition is most often encountered in partial forms.

It is named after physiologist Charles-Édouard Brown-Séquard, who first described the condition in 1850.^[1]

Presentation and pathophysiology

The syndrome is frequently encountered in clinical practice, but only rarely presents in its classical form^[2] because most lesions are irregular;^[3] partial hemisection is common, but complete hemisection is rare.^[4] The development of characteristic pathology is preceded by a period of spinal shock.^[5]

Neuroanatomy

The hemisection of the spinal cord produces the classical triad characterising this syndrome by disrupting the following three structures of the spinal cord:

• Corticospinal tract - the "pyramidal" tract containing upper motor neurons mediates voluntary movements of skeletal muscle. It consists of two subdivisions: the lateral corticospinal tract which is situated in the lateral funiculus, controls musculature associated with the limbs and does not decussate within the spinal cord; and the anterior corticospinal tract which is situated in the anterior funiculus, controls the musculature of the trunk and does decussate within the spinal cord.
• Posterior funiculus - posterior anatomical division of the white matter of the spinal cord exclusively containing axons of 1st-order neurons of the dorsal column–medial lemniscus pathway which conveys sensory stimuli regarding fine (discriminative) touch, proprioception, and vibratory sense from the trunk and limbs. These do not decussate within the spinal cord.
• Spinothalamic tract - consists of two subdivisions: the lateral spinothalamic tract which is situated within the lateral funiculus and conveys sensory stimuli regarding pain, temperature, and pressure; and the anterior spinothalamic tract which is situated within the anterior funiculus and conveys sensory stimuli concerning crude (non-discriminative) touch and pressure information. Both tracts decussate within the spinal cord.

Motor

Lesion on the patient's right

1. loss of all sensation, hypotonic paralysis
2. spastic paralysis and loss of vibration and proprioception (position sense) and fine touch
3. loss of pain and temperature sensation

At the level of the lesion, destruction of the anterior gray column and potentially also of the anterior (motor) root of the corresponding spinal nerve results in destruction of lower motor neurons of the spinal segment on the affected side, causing flaccid paralysis and consequent muscle atrophy of the corresponding myotome.^[5]

Disruption of the upper motor neuron corticospinal tract produces ipsilateral spastic paralysis below the level of the lesion.^[2][4] Spasticity is a consequence of disruption of ipsilateral extrapiramidal tracts.^[5]

Reflexes

BSS is associated with ipsilateral Babinski sign and possibly (depending upon the level of the lesion) with loss of ipsilateral cremasteric reflex, and abdominal reflex.^[5]

Sensory

At the level of the lesion, destruction of the posterior (sensory) root of the corresponding spinal nerve causes complete loss of sensation (anaesthesia) of the corresponding dermatome.^[5]

Disruption of the dorsal column pathway causes ipsilateral loss of fine (discriminative) touch, vibration, and proprioceptive perception.^[4]

Disruption of the spinothalamic tract causes contralateral loss of pain, temperature, and crude (non-discriminative) touch sensation loss starting from 2-3 spinal cord segments inferior to the level of the lesion (because 2nd-order axons of the spinothalamic tract decussate obliquely).^[5]

Causes

Brown-Séquard syndrome may be caused by trauma (either blunt trauma or penetrative injury),^{[citation needed]} spinal cord tumors, syringomyelia, hematomyelia,^[3] ischemia (obstruction of a blood vessel), infection (e.g. spinal tuberculosis,^{[citation needed]} human herpesvirus 3^[2]) or autoimmune disease (e.g. multiple sclerosis). The most common cause is penetrating trauma such as gunshot injury or a stab wound to the spinal cord.^{[citation needed]}

History

Charles-Édouard Brown-Séquard studied the anatomy and physiology of the spinal cord. He described this injury after observing spinal cord trauma which happened to farmers while cutting sugar cane in Mauritius. French physician, Paul Loye, attempted to confirm Brown-Séquard's observations on the nervous system by experimentation with decapitation of dogs and other animals and recording the extent of each animal's movement after decapitation.^[6]