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Brown-Sequard Syndrome

  • Author: Carol Vandenakker-Albanese, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
 
Updated: Mar 28, 2014
 

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.

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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.

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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.

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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.[2, 3]

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.[4] 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 [5]
  • Herniation of the spinal cord through a dural defect (idiopathic or posttraumatic)
  • Epidural hematoma
  • Vertebral artery dissection
  • Transverse myelitis
  • Radiation
  • Type II decompression sickness
  • Intravenous drug use
  • Tuberculosis
  • Ossification of the ligamentum flavum [6]
  • Meningitis
  • Empyema
  • Herpes zoster
  • Herpes simplex
  • Syphilis
  • Ischemia
  • Hemorrhage - Including spinal subdural/epidural and hematomyelia
  • Chiropractic manipulation – Rare, but reported [7, 8]
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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.[9] 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.[10]

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Prognosis

Prognosis for significant motor recovery in Brown-Séquard syndrome is good.[10] 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[11] :

  • 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.[12] ) 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.[13]

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.

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Contributor Information and Disclosures
Author

Carol Vandenakker-Albanese, MD Professor, Department of Physical Medicine and Rehabilitation, University of California Davis Health System; Physical Medicine and Rehabilitation Residency Director, University of California, Davis, School of Medicine

Carol Vandenakker-Albanese, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, North American Spine Society, American College of Sports Medicine, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Coauthor(s)

Holly Zhao, MD, PhD Assistant Professor of Clinical Physical Medicine and Rehabilitation, University of California Davis Health System

Holly Zhao, MD, PhD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Physical Medicine and Rehabilitation, American Medical Association, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans

Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Michael T Andary, MD, MS Professor, Residency Program Director, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine

Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists

Disclosure: Allergan Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching

Michael S Beeson, MD, MBA, FACEP Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center

Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Samuel M Keim, MD Associate Professor, Department of Emergency Medicine, University of Arizona College of Medicine

Samuel M Keim, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Public Health Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Elizabeth A Moberg-Wolff, MD Associate Professor, Department of Physical Medicine and Rehabilitation, Children's Hospital of Wisconsin, Medical College of Wisconsin

Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation

Disclosure: Medtronic Neurological Grant/research funds Speaking and teaching

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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