Brown-Sequard Syndrome 

Charles Edouard Brown-Séquard (1817-1894) was a remarkable man who is remembered primarily for his contribution to neurology. He was a prolific researcher and writer, publishing 577 papers during his lifetime. The finding for which he became famous carries his name. He first published a description of lateral hemisection of the spinal cord in 1849. His description of ipsilateral paralysis and hyperesthesia with loss of sensation in the contralateral limb was based on numerous animal experiments and collected human cases with autopsy confirmation.

Brown-Séquard syndrome is defined as an incomplete lesion of the spinal cord characterized by ipsilateral upper motor neuron paralysis and loss of proprioception, with contralateral loss of pain and temperature sensation. A zone of partial preservation or segmental ipsilateral lower motor neuron weakness and analgesia may be noted. Loss of ipsilateral autonomic function can result in Horner syndrome. As an incomplete spinal cord syndrome, the clinical presentation of Brown-Séquard syndrome may range from mild to severe neurologic deficit.

Brown-Séquard – plus syndrome is a term often used to describe less pure forms of the syndrome.^[1]

Related eMedicine topics:

Brown-Sequard Syndrome [Emergency Medicine]

Spinal Cord Trauma and Related Diseases

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Resource Center Spinal Disorders

The pathophysiology of Brown-Séquard syndrome is damage to or loss of ascending and descending spinal cord tracts on one side of the spinal cord. Spinal cord anatomy accounts for the clinical presentation. The motor fibers of the corticospinal tracts cross at the junction of the medulla and spinal cord. The ascending dorsal column carrying sensation of vibration and position runs ipsilateral to the roots of entry and crosses above the spinal cord in the medulla. The spinothalamic tracts convey sensations of pain, temperature, and crude touch from the contralateral side of the body. At the site of spinal cord injury (SCI), nerve roots and/or anterior horn cells also may be affected.

The structural and ultrastructural changes that occur in the cord have been studied in animals and postmortem human subjects. Scattered petechial hemorrhages develop in the gray matter and enlarge and coalesce by 1 hour postinjury. Subsequent development of hemorrhagic necrosis occurs within 24-36 hours. White matter shows petechial hemorrhage at 3-4 hours. Myelinated fibers and long tracts show extensive structural damage.

Frequency

United States

The true incidence of Brown-Séquard syndrome is not known. No national database exists to record all spinal cord syndromes resulting from traumatic and nontraumatic etiologies. The incidence of traumatic SCIs in the United States is estimated at 11,000 new cases per year, with Brown-Séquard syndrome accounting for 2-4% of the traumatic injuries. Prevalence of all SCIs in the United States is estimated to be approximately 247,000 persons.^[2]

Related Medscape topic:

Resource Center Trauma

International

International incidence is unknown.

Mortality/Morbidity

• Acute mortality rates are measured for all traumatic SCIs without differentiation according to level or completeness. These figures do not include nontraumatic cases and do not differentiate the incomplete spinal cord syndromes. Incomplete tetraplegia has been the most frequent neurologic category reported to the database since 2000. The mortality rate is 5.7% during the initial hospitalization if no surgery is performed, and 2.7% if surgical intervention is performed. Mortality prior to hospitalization is not known but has decreased with the advancement of emergency medical services. Long-term mortality has been studied extensively for complete and incomplete spinal cord lesions, based on age at injury and neurologic level. Statistics on mortality ratios, life expectancy, and the underlying and secondary causes of death are available from the National Model Systems Database.
• Morbidity following any SCI, regardless of etiology, is related to loss of motor, sensory and autonomic function as well as to common secondary medical complications. Although prognosis for neurologic recovery is better in the incomplete syndromes than it is in complete SCIs, complete recovery by the time of hospital discharge is less than 1%. The most prevalent medical complication is a pressure ulcer, followed by pneumonia, urinary tract infection, deep vein thrombosis, pulmonary embolus, and postoperative infection.

Race

The SCI database indicates that since 2000, 63% of cases of Brown-S é quard syndrome have occurred in the white population; 22.7%, in African Americans; 11.8%, in Hispanics; and 2.4%, in other racial/ethnic groups.

Sex

Various demographic studies have consistently shown a greater frequency of SCI in males than in females. This finding primarily reflects traumatic injury data and may not reflect the frequency of nontraumatic etiologies.

Age

Population-based studies reveal that SCI occurs primarily in persons aged 16-30 years, but the mean age has increased over the past 30 years. Since 2000, the average age at injury is 38 years. If other etiologies of Brown-S é quard syndrome were to be considered, mean age would increase further.^[3]