Brown-Sequard Syndrome 

Updated: Sep 06, 2018
Author: Carol Vandenakker-Albanese, MD; Chief Editor: Stephen Kishner, MD, MHA 

Overview

Background

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. (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.[1]

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.

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.

Anatomy

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.

Pathophysiology

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.[2]

Etiology

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.[3, 4]

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.[5] 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[6]

  • Cervical spondylosis

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

  • Epidural hematoma

  • Vertebral artery dissection[7]

  • Transverse myelitis

  • Radiation

  • Type II decompression sickness

  • Intravenous drug use

  • Tuberculosis

  • Ossification of the ligamentum flavum[8]

  • Meningitis

  • Empyema

  • Herpes zoster

  • Herpes simplex

  • Syphilis

  • Ischemia

  • Hemorrhage - Including spinal subdural/epidural and hematomyelia

  • Chiropractic manipulation – Rare, but reported[9, 10]

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.[11]

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).[12]

Epidemiology

Occurrence in the United States

Brown-Séquard syndrome is rare, although its true incidence is unknown. 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 12,000 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 273,000 persons.[13] International incidence of the syndrome is unknown.

Race-, sex-, and age-related demographics

The SCI database indicates that since 2010, 67% of cases of spinal cord injury have occurred in the white population, 24.4% in African Americans, 7.9% in Hispanics, and 0.7% 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 2010, the average age at injury has been 42.6 years for persons with traumatic SCI. The average age of individuals with Brown-Séquard syndrome is 40 years.[14]

Prognosis

Prognosis for significant motor recovery in Brown-Séquard syndrome is good.[14] 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[15] :

  • 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 central cord or Brown-Séquard syndrome, younger patients with 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.[16] ) 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.[17]

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 (40.6% of traumatic SCIs) reported to the National Spinal Cord Injury Database since 2010. 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.

 

Presentation

History

Clinical history often reflects the etiology of Brown-Séquard syndrome. Onset of symptoms may be acute or gradually progressive. Complaints are related to hemiparesis or hemiparalysis and sensory changes, paresthesias, or dysesthesias in the contralateral limb(s). Isolated weakness or sensory changes may be reported.

Complete hemisection, causing classic clinical features of pure Brown-Séquard syndrome, is rare. Incomplete hemisection causing Brown-Séquard syndrome plus other signs and symptoms is more common. These symptoms may consist of findings from posterior column involvement such as loss of vibratory sensation.

Physical Examination

Diagnosis and identification of Brown-Séquard syndrome is based on physical examination findings. 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

Try to differentiate levels of sensation loss, motor loss, temperature loss, and vibratory sense loss. Evaluate bilateral versus unilateral neurologic findings when determining level of loss.

Motor examination in patients with Brown-Séquard syndrome reveals spastic weakness or paralysis with upper motor neuron signs of increased tone, hyperreflexia, clonus, and a Hoffmann sign on 1 side of the body. Motor strength of key muscles representing cervical and lumbar spinal root levels should be graded on the standard 0-5 scale. Special care must be taken to test in positions with gravity eliminated and against gravity.

The sensory examination is notable for contralateral decreased sensations of light touch and hot or cold. Sensory function should be recorded in representative dermatomes from C2-S4/5 for absent, impaired, or normal sensations of light touch and pinpricks.[18]

Classification

Motor and sensory findings can be classified according to the American Spinal Injury Association (ASIA) standard neurologic classification of SCI (see the image below). The neurologic level is defined as the most caudal segment with normal function. Complete or incomplete assessment is based on sensory or motor function in S4-S5.

American Spinal Injury Association (ASIA) standard American Spinal Injury Association (ASIA) standard neurologic classification of spinal cord injury.

The ASIA Impairment Scale reflects the degree of incomplete injury based on motor and sensory function below the neurologic level. (See the image below.)

American Spinal Injury Association (ASIA) Impairme American Spinal Injury Association (ASIA) Impairment Scale.
 

DDx

Diagnostic Considerations

Conditions to consider in the differential diagnosis of Brown-Séquard syndrome include the following:

  • Spinal infection

  • Vascular malformation

  • Spinal cord tumor, primary or metastatic

  • Spinal cord herniation

  • Postradiation spinal cord dysfunction

  • Eccentric disk herniation with cord compression

  • Cervical disc disease

  • Decompression sickness

Differential Diagnoses

 

Workup

Approach Considerations

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. Purified protein derivative and sputum for acid-fast bacilli should be ordered if tuberculosis is suggested as an etiology.

If the cause of the SCI was traumatic, do not fail to consider that other injuries may be present as well. One commonly neglected area is the abdomen; the possibility of intra-abdominal injury must be taken into account. Always consider imaging of the abdomen/pelvis when the spinal cord is injured.

Recognize that hypotension may be the result of something other than neurogenic shock. If, for example, the spinal injury was caused by trauma, hypotension may result from hemorrhagic causes.

Bladder catheterization

Bladder catheterization may identify varying degrees of bladder dysfunction in some cases.

Lumbar puncture

Lumbar puncture is performed only for the diagnosis of specific, suggested etiologies. The diagnosis of multiple sclerosis, transverse myelitis, tumor, or tuberculosis may require lumbar puncture with laboratory analysis of cerebral spinal fluid. Tumor diagnosis may require open biopsy with tissue pathology or computed tomography (CT) scan–guided needle biopsy.

Imaging Studies

Radiography

Radiographic studies help to confirm the diagnosis and determine the etiology of Brown-Séquard syndrome. Plain films always are required in acute trauma to the spine, but more information usually is obtained by newer techniques.

Spinal plain radiographs may depict bony injury in penetrating or blunt trauma. Lateral mass fracture may cause Brown-Séquard syndrome after blunt injury.

MRI

Magnetic resonance imaging (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. No contrast is necessary for acute injury, but if an intradural etiology is suspected, a gadolinium or phase-contrast cine MRI scan may be helpful.[19, 20]

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.[21, 22]

Other

The suggested etiology of Brown-Séquard syndrome can dictate the use of imaging studies other than radiography, CT scanning, and MRI. Angiography is helpful in identifying vascular malformation. Nuclear medicine scans may be necessary to identify infectious or inflammatory causes.

 

Treatment

Approach Considerations

Special care must be taken in preparing a life-care plan for a patient with Brown-Séquard syndrome. The incompleteness of the syndrome in conjunction with a good prognosis for recovery makes determination of needs over a lifetime difficult. If evaluated too early, needs may be grossly overestimated. If evaluation is performed at the time of maximal function, the expected difficulties and changes associated with aging with disability must not be forgotten.

Any SCI, regardless of degree of completeness, results in significant alterations in function of the respiratory, cardiovascular, digestive, urinary, musculoskeletal, and integumentary systems. Decreased pulmonary function, altered cardiovascular dynamics, neurogenic bowel and bladder dysfunctions, hypercalcemia, osteoporosis, heterotopic ossification, and insensate skin may not be avoidable, but secondary medical complications often are preventable with expert care. The following secondary complications need to be addressed with aggressive preventive measures and early treatment:

  • Development of pulmonary infections and respiratory insufficiency

  • Uncontrolled autonomic dysreflexia

  • Bowel impaction

  • Urinary tract infections

  • Pressure ulcers

Avoidance of medical complications reduces morbidity and mortality; it also speeds the rehabilitation process.

Pharmacologic therapy

Medication use is dependent on the secondary effects of SCI. Medication may be indicated for spasticity, pain, or a number of other possible complications. In general, persons with Brown-Séquard syndrome regain significant function, and many medications are not needed long term.

Nasogastric tube insertion

Nasogastric (NG) tube insertion and subsequent low-wall suction may help to prevent aspiration. Additionally, these patients are prone to developing ileus in the acute stage.

Cervical spine immobilization

Cervical spine immobilization, or lower dorsal vertebra immobilization, is required with trauma or suspicion of an unstable spine. Hard-collar immobilization or Gardner Wells tongs may be required if cervical fracture/injury is identified.

Patient transfer

Transfer to a level I trauma center or to a facility with expertise in the care of spinal cord injuries is appropriate; however, transfer should not impede the overall evaluation of these patients, including assessment for additional injuries.

Prevention

A number of community outreach programs have been developed to educate young people about the risks of traumatic injury associated with certain behaviors. Results of such injury, such as SCI, are described in detail, and preventive measures are outlined. These programs have been found to have a positive impact on the rate of injury.

Prehospital Care

The key to successful prehospital care of patients with Brown-Séquard syndrome is to suspect a cervical or other spinal injury. A low threshold for cervical spine/backboard immobilization is appropriate. One issue with prehospital evaluation of cervical spine injury is the potential for assumption of a complete spinal cord lesion rather than an incomplete lesion. Prehospital providers must be educated regarding the findings of incomplete cord syndromes and how to make a brief assessment of complete versus incomplete cord lesion.

Emergency Department Care

Care in the emergency department (ED) consists of a thorough evaluation, including a neurologic examination for level of injury. Careful cervical spine/dorsal spine immobilization is necessary, with elimination of neck movement.

The nature of sensory loss makes investigation of other injuries more difficult. This mandates a thorough and complete physical examination, with imaging studies used to supplement the exam.

Administer steroids in a timely manner: Initiate steroids promptly on the basis of the initial ED evaluation.

Physical Therapy

Physical therapy intervention starts in the acute care phase of treatment.[23] 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 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.

Prior to discharge, the patient's home is evaluated for accessibility and modifications, as well as for the need for adaptive equipment. The need for orthotics is assessed and recommended. After fitting, training with the orthotic device is vital to functional use.

Because neurologic recovery often continues following discharge from acute inpatient rehabilitation, physical therapy should continue in the outpatient setting. Frequent reassessments are indicated to set new functional goals and to modify treatment as needed. Patients and caregivers should be instructed in home exercise programs that are designed to maintain the patients’ strength, flexibility, and balance.

Occupational Therapy

To enable patients with Brown-Séquard syndrome to regain as much independence as possible in activities of daily living, occupational therapy is essential. 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.

Patients with Brown-Séquard syndrome typically show neurologic improvement over the course of the first year after onset and may advance through several stages of independence in performing activities of daily living. Occupational therapy should be continued for as long as the patient shows improvement in functional status.

Recreational Therapy

A person's leisure and recreational needs often increase after a significant change in physical function. Although patients with Brown-Séquard syndrome may regain more function than do most patients with SCI, consideration of recreational needs is still important. Premorbid interests are assessed and incorporated into the development of adaptive sports, leisure activities, and a recreational program.

The recreational therapist re-introduces a person with a disability into the community to develop the confidence needed for re-integration into society. The therapist also serves as a source of information and as a liaison to community programs for the disabled.

Spinal Reduction, Stabilization, and Decompression

Surgical intervention in traumatic SCI has been controversial, focusing primarily on spinal stability.[17, 24] 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 more 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.[21]

Consultations

Acute consultations are based on patient symptomatology and the etiology of the Brown-Séquard syndrome. Although patients with Brown-Séquard syndrome frequently regain bladder function, consultation with a urologist is required most commonly for evaluation of neurogenic bladder dysfunction.[25] In addition, it is essential that physical medicine and rehabilitation specialists be consulted early on in the initial stages of patient care.

Other specialists who should be available for consultation over the course of the patient's rehabilitation include the following:

  • Orthopedist

  • Neurosurgeon

  • General surgeon

  • Hematologist-oncologist

  • Infectious disease specialist

  • Pulmonologist

  • Cardiologist

  • Gastroenterologist

  • Neurologist

  • Psychiatrist

  • General medicine specialist

  • Dentist

Long-Term Monitoring

Basic medical follow-up care for SCI is recommended every 1-3 years. The suggested assessments include full history and physical (eg, weight, vital signs), vital capacity if the injury level is above T6, routine blood tests, neurologic evaluation with ASIA scoring, and cardiac risk assessment. Urologic evaluation also is recommended, but it is not necessary if a patient with Brown-Séquard syndrome has regained normal bladder function.

Brown-Séquard syndrome carries a more favorable prognosis than do most SCIs, with ongoing neurologic recovery occurring for up to 2 years following the injury. As long as a person's neurologic status is improving and his/her rehabilitation goals change, ongoing physical and occupational therapy are indicated. Following achievement of an optimal functional level, assessment by a physical therapist, occupational therapist, psychosocial counselor, and therapeutic recreation specialist is recommended every 1-3 years.

In the patient who recovers ambulatory function, regular evaluation of any orthotics or assistive devices also is necessary, to ensure safety and prevent skin breakdown.

 

Medication

Medication Summary

The use of medications for Brown-Séquard syndrome is dependent on the etiology and acuity of onset. Acute treatment of traumatic SCI involves immediate dosing of methyl prednisolone. Acute immobility that is unrelated to a bleed requires anticoagulation therapy, if not contraindicated. Gastrointestinal protection is strongly recommended.

Other medications are used to manage symptoms and complications as needed, including antibiotics, antispasmodics, pain medications, and laxatives.

Corticosteroids

Class Summary

Multiple studies have demonstrated improved outcomes for patients with traumatic SCIs who were given high-dose steroids early in the clinical course. (Although the previously mentioned study by Pollard and Apple did not find these results in incomplete cervical SCIs.[16] ) These drugs have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Methylprednisolone (A-Methapred, Medrol, Solu-Medrol, Depo-Medrol)

Methylprednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.