Brown-Sequard Syndrome

Updated: Sep 14, 2022
  • Author: Carol Vandenakker-Albanese, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
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Practice Essentials

Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by a clinical picture reflecting hemisection injury of the spinal cord, often in the cervical cord region. [1, 2] (See Presentation.)

Patients with Brown-Séquard syndrome suffer from ipsilateral upper motor neuron paralysis and loss of proprioception, as well as 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. (See Etiology, Presentation, and Workup.)

As an incomplete spinal cord syndrome, the clinical presentation of Brown-Séquard syndrome may range from mild to severe neurologic deficit. (See Presentation.)

Brown-Séquard–plus syndrome

The pure Brown-Séquard syndrome reflecting hemisection of the cord is not often observed. A clinical picture composed of fragments of the syndrome or of the hemisection syndrome plus additional symptoms and signs is more common. These less-pure forms of the disorder are often referred to as Brown-Séquard–plus syndrome. [3]

Interruption of the lateral corticospinal tracts, the lateral spinal thalamic tract, and at times the posterior columns produces a picture of a spastic, weak leg with brisk reflexes and a strong leg with loss of pain and temperature sensation. Note that spasticity and hyperactive reflexes may not be present with an acute lesion.

Signs and symptoms of Brown-Séquard syndrome

Partial Brown-Séquard syndrome is characterized by asymmetrical paresis, with hypalgesia more marked on the less paretic side. Pure Brown-Séquard syndrome (rarely seen in clinical practice) is associated with the following:

  • Interruption of the lateral corticospinal tracts - Ipsilateral spastic paralysis below the level of the lesion and Babinski sign ipsilateral to the lesion (abnormal reflexes and Babinski sign may not be present in acute injury)
  • Interruption of posterior white column - Ipsilateral loss of tactile discrimination, as well as vibratory and position sensation, below the level of the lesion
  • Interruption of lateral spinothalamic tracts - Contralateral loss of pain and temperature sensation; this usually occurs 2-3 segments below the level of the lesion

Workup in Brown-Séquard syndrome

The diagnosis of Brown-Séquard syndrome is made on the basis of history and physical examination. Laboratory work is not necessary to evaluate for the condition but may be helpful in following the patient's clinical course. Laboratory studies may also be useful in nontraumatic etiologies, such as infectious or neoplastic causes.

Bladder catheterization may identify varying degrees of bladder dysfunction in some cases. Lumbar puncture is performed only for the diagnosis of specific, suggested etiologies.

Imaging studies in Brown-Séquard syndrome include the following:

  • Radiography - Radiographic studies help to confirm the diagnosis and determine the etiology of Brown-Séquard syndrome
  • Magnetic resonance imaging (MRI) - MRI is very useful in determining the exact structures that have been damaged in Brown-Séquard syndrome, as well as in identifying nontraumatic etiologies of the disorder
  • Computed tomography (CT) scanning - In persons who are unable to have an MRI scan performed, a CT myelogram is the study of choice; imaging is expected to reveal destruction of nerve tissue localized to one side of the spinal cord [4, 5]

Management of Brown-Séquard syndrome

Physical therapy

Physical therapy intervention starts in the acute care phase of treatment. [6] Therapy goals include the following:

  • Maintaining strength in neurologically intact muscles
  • Maintaining range of motion in joints
  • Preventing skin breakdown by proper positioning and weight shifting
  • Improving respiratory function by positioning and breathing exercises
  • Achieving early mobilization to increase tolerance of the upright position
  • Providing emotional and educational support for the patient and his/her family

As a person with spinal cord injury (SCI) advances through acute rehabilitation, physical therapy addresses mobility issues. Functional movement starts with bed mobility, followed by transfers, wheelchair mobility, and, in many cases of Brown-Séquard syndrome, ambulation. Appropriate equipment must be prescribed, and the proper use of the equipment should be taught to the patient and caregivers.

Occupational therapy

Upper extremity function is assessed carefully and then is used to learn new techniques, with or without the use of adaptive equipment, for the performance of oral-facial hygiene, feeding, and dressing. Head control, upper extremity strength, and trunk balance are developed to enable the patient to accomplish these tasks.

Transfers and wheelchair mobility are addressed in conjunction with the physical therapist. Driving assessment, adaptations, and training are performed when appropriate.

Surgical therapy

The need for prompt reduction of any spinal deformity is well accepted. The reduction can be achieved either posturally or operatively.

Stabilization of the reduced spine to prevent further injury to the cord is controversial. Stability may come from direct surgical repair with bone grafting and (often) instrumentation or from natural healing or autofusion in an orthosis. Most stable spinal injuries are treated nonoperatively, while unstable injuries are treated surgically.

Surgical decompression of the spinal canal may be indicated for an incomplete syndrome in which residual compression is present. Nontraumatic etiologies of Brown-Séquard syndrome usually involve mechanical compression or herniation of the spinal cord and require surgical decompression. [4]

Patient education

Patients must receive extensive education on body system functions, the social and psychological effects of their condition, coping strategies, and community re-integration.



Spinal cord anatomy accounts for the clinical presentation of Brown-Séquard syndrome. The motor fibers of the corticospinal tracts cross at the junction of the medulla and spinal cord. The ascending dorsal column, carrying the sensations 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.



Brown-Séquard syndrome results from damage to or loss of ascending and descending spinal cord tracts on 1 side of the spinal cord. 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.

A study by Saadon-Grosman et al of two groups of patients—one with cervical sensory Brown-Séquard syndrome and one with patients prior to and following surgical repair of a cervical disk protrusion—found evidence that reduced sensation in these patients was associated not with signal decrease but with gradient discontinuity at the primary somatosensory cortex and the supplementary motor area. [7]



Traumatic causes

Brown-Séquard syndrome can be caused by any mechanism resulting in damage to 1 side of the spinal cord. Multiple causes of Brown-Séquard syndrome have been described in the literature. The most common cause remains traumatic injury, often a penetrating mechanism, such as a stab or gunshot wound or a unilateral facet fracture and dislocation due to a motor vehicle accident or fall. [8, 9]

More unusual etiologies that have been reported include assault with a pen, removal of a cerebrospinal fluid drainage catheter after thoracic aortic surgery, and injury from a blowgun dart. [10] Traumatic injury may also be the result of blunt trauma or pressure contusion.

Nontraumatic causes

Numerous nontraumatic causes of Brown-Séquard syndrome have also been reported, including the following:

  • Tumor (primary or metastatic)

  • Multiple sclerosis

  • Disk herniation [11]

  • Herniation of the spinal cord through a dural defect (idiopathic or posttraumatic)

  • Epidural hematoma

  • Vertebral artery dissection [12]

  • Transverse myelitis

  • Radiation

  • Type II decompression sickness

  • Intravenous drug use

  • Tuberculosis

  • Ossification of the ligamentum flavum [13]

  • Meningitis

  • Empyema

  • Herpes zoster

  • Herpes simplex

  • Syphilis

  • Ischemia

  • Hemorrhage - Including spinal subdural/epidural and hematomyelia

  • Chiropractic manipulation – Rare, but reported [14, 15]

A literature review by Gunasekaran et al found that out of 37 patients with cervical intradural disk herniation, a rare condition, 43.2% had Brown-Séquard syndrome, while 10.8% had Horner syndrome. [16]

A retrospective study by Ronzi et al looked at patients with acute traumatic SCI associated with cervical spinal canal stenosis, in whom spinal stability was retained. The investigators determined that of the 78.6% of patients with a clinical syndrome, the greatest proportion had Brown-Séquard–plus syndrome (30.9% of patients). [17]



Occurrence in the United States

Brown-Séquard syndrome is rare, although its true incidence is uncertain. The incidence of traumatic SCIs in the United States is estimated at 17,800 new cases per year, with Brown-Séquard syndrome resulting from 2-4% of the injuries. Prevalence of all SCIs in the United States is estimated to be approximately 294,000 persons. [18]

Using the National Spinal Cord Injury Model Systems Database, Engel-Haber et al determined that the incomplete SCI syndromes central cord syndrome, anterior cord syndrome, and Brown-Séquard syndrome make up 14%, 6.5%, and 2% of all traumatic SCIs, respectively. Among 1649 individuals in the cohort who had incomplete tetraplegia, those figures were found to be 30%, 10%, and 3%, respectively. [19]  The international incidence of Brown-Séquard syndrome is unknown.

Race-, sex-, and age-related demographics

The SCI database indicates that since 2015, 59% of cases of spinal cord injury have occurred in the white population, 23.9% in African Americans, 12.8% in Hispanics, and 1.4% in other racial/ethnic groups.

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.

Population-based studies reveal that SCI occurs primarily in persons aged 16-30 years, but the mean age has increased over the last few decades. Since 2015, the average age at injury has been 43 years for persons with traumatic SCI. The average age of individuals with Brown-Séquard syndrome is 40 years. [20]



Prognosis for significant motor recovery in Brown-Séquard syndrome is good. [20] One half to two thirds of the 1-year motor recovery occurs within the first 1-2 months following injury. Recovery then slows but continues for 3-6 months and has been documented to progress for up to 2 years following injury.

The most common pattern of recovery includes the following [21] :

  • Recovery of the ipsilateral proximal extensor muscles prior to that of the ipsilateral distal flexors

  • Recovery from weakness in the extremity with sensory loss before recovery occurs in the opposite extremity

  • Recovery of voluntary motor strength and a functional gait within 1-6 months

A retrospective review by Pollard and Apple of 412 patients with traumatic, incomplete cervical SCIs found that the most important prognostic variable relating to neurologic recovery was completeness of the lesion. If the cervical spinal cord lesion is incomplete, such as in central cord or Brown-Séquard syndrome, younger patients will have a more favorable prognosis for recovery.

Recovery in the study was not linked to high-dose steroid administration, early surgical intervention on a routine basis, or surgical decompression in patients with stenosis who were without fracture. (Other studies, however, have demonstrated improved outcomes for patients with traumatic SCIs who were given high-dose steroids early in the clinical course. [22] ) Surgical treatment of stenosis with myelopathy or incomplete spinal cord injury, including Brown-Séquard syndrome, has been shown to halt progressive loss of neurological function. [23]

Studies suggest that spared descending motor axons in the contralateral cord may mediate much of the motor recovery. Most individuals with incomplete injuries at the time of initial examination recover the ability to ambulate.

Morbidity and mortality

Potential long-term complications of Brown-Séquard syndrome are similar to those associated with aging and SCI. Lower extremity problems related to ambulation may increase, but this phenomenon has not been documented in the literature.

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 at hospital discharge has been the most frequent neurologic category (47.2% of traumatic SCIs) reported to the National Spinal Cord Injury Database since 2015. There are no data specific to Brown-Séquard syndrome.

The mortality rate for incomplete tetraplegia in general is 5.7% during the initial hospitalization if no surgery is performed and is 2.7% if surgical intervention is performed. Mortality prior to hospitalization is not known but has decreased with the advancement of emergency medical services.

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 pressure ulcer, followed by pneumonia, urinary tract infection, deep venous thrombosis, pulmonary embolus, and postoperative infection.