eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Brown-Sequard Syndrome

Author: Carol Vandenakker-Albanese, MD, Director, Post-Polio Clinic, Department of Physical Medicine and Rehabilitation, University of California at Davis Health System; Physical Medicine and Rehabilitation Residency Director, University of California at Davis
Coauthor(s): Holly Zhao, MD, PhD, Assistant Professor of Clinical Physical Medicine and Rehabilitation, University of California Davis Health System
Contributor Information and Disclosures

Updated: Jul 31, 2008

Introduction

Background

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

Related Medscape topic:
Resource Center Spinal Disorders

Pathophysiology

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

Clinical

History

Clinical history often reflects the etiology of Brown-S é quard 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.

Physical

Diagnosis and identification of Brown-Séquard syndrome is based on physical examination findings. In clinical practice, the pure classic syndrome is rarely seen. Motor examination reveals spastic weakness or paralysis with upper motor neuron signs of increased tone, hyperreflexia, clonus, and a Hoffmann sign on one 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.4

The findings then can be classified according to the American Spinal Injury Association (ASIA) standard neurologic classification of SCI. 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. The ASIA impairment scale reflects the degree of incomplete injury based on motor and sensory function below the neurologic level (see Images 1-2).

Causes

Brown-Séquard syndrome can be caused by any mechanism resulting in damage to one 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. More unusual etiologies that have been reported include assault with a pen, removal of a cerebrospinal fluid drainage catheter after thoracic aortic surgery, and a blowgun dart injury.5 Traumatic injury may also be the result of blunt trauma or pressure contusion.

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

  • Tumor (primary or metastatic)
  • Multiple sclerosis
  • Disk herniation
  • 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 flavum6

More on Brown-Sequard Syndrome

Overview: Brown-Sequard Syndrome
Differential Diagnoses & Workup: Brown-Sequard Syndrome
Treatment & Medication: Brown-Sequard Syndrome
Follow-up: Brown-Sequard Syndrome
Multimedia: Brown-Sequard Syndrome
References

References

  1. McCarron MO, Flynn PA, Pang KA, et al. Traumatic Brown-Séquard-plus syndrome. Arch Neurol. Sep 2001;58(9):1470-2. [Medline][Full Text].

  2. Spinal Cord Injury Information Network. Facts and Figures at a Glance. 2008;[Full Text].

  3. McKinley W, Santos K, Meade M, et al. Incidence and outcomes of spinal cord injury clinical syndromes. J Spinal Cord Med. 2007;30(3):215-24. [Medline][Full Text].

  4. Hayes KC, Hsieh JT, Wolfe DL, et al. Classifying incomplete spinal cord injury syndromes: algorithms based on the International Standards for Neurological and Functional Classification of Spinal Cord Injury Patients. Arch Phys Med Rehabil. May 2000;81(5):644-52. [Medline].

  5. Moin H, Khalili HA. Brown Séquard syndrome due to cervical pen assault. J Clin Forensic Med. Apr 2006;13(3):144-5. [Medline].

  6. Chen PY, Lin CY, Tzaan WC, et al. Brown-Sequard syndrome caused by ossification of the ligamentum flavum. J Clin Neurosci. Sep 2007;14(9):887-90. [Medline].

  7. Clatterbuck RE, Belzberg AJ, Ducker TB. Intradural cervical disc herniation and Brown-Séquard's syndrome. Report of three cases and review of the literature. J Neurosurg. Apr 2000;92(2 Suppl):236-40. [Medline].

  8. Jacobsohn M, Semple P, Dunn R, et al. Stab injuries to the spinal cord: a retrospective study on clinical findings and magnetic resonance imaging changes. Neurosurgery. Dec 2007;61(6):1262-6; discussion 1266-7. [Medline].

  9. Parmar H, Park P, Brahma B, et al. Imaging of idiopathic spinal cord herniation. Radiographics. Mar-Apr 2008;28(2):511-8. [Medline].

  10. Miranda P, Gomez P, Alday R, et al. Brown-Sequard syndrome after blunt cervical spine trauma: clinical and radiological correlations. Eur Spine J. Aug 2007;16(8):1165-70. [Medline].

  11. Winchester PK, Williamson JW, Mitchell JH. Cardiovascular responses to static exercise in patients with Brown-Séquard syndrome. J Physiol. Aug 15 2000;527 Pt 1:193-202. [Medline][Full Text].

  12. Massicotte EM, Montanera W, Ross Fleming JF, et al. Idiopathic spinal cord herniation: report of eight cases and review of the literature. Spine. May 1 2002;27(9):E233-41. [Medline].

  13. Kohno M, Takahashi H, Yamakawa K, et al. Postoperative prognosis of Brown-Séquard-type myelopathy in patients with cervical lesions. Surg Neurol. Mar 1999;51(3):241-6. [Medline].

  14. Scivoletto G, Cosentino E, Morganti B, et al. Clinical prognostic factors for bladder function recovery of patients with spinal cord and cauda equina lesions. Disabil Rehabil. May 11 2007;1-8. [Medline].

  15. Pollard ME, Apple DF. Factors associated with improved neurologic outcomes in patients with incomplete tetraplegia. Spine. Jan 1 2003;28(1):33-9. [Medline].

  16. Little JW, Halar E. Temporal course of motor recovery after Brown-Sequard spinal cord injuries. Paraplegia. Feb 1985;23(1):39-46. [Medline].

  17. Antich PA, Sanjuan AC, Girvent FM, et al. High cervical disc herniation and Brown-Sequard syndrome. A case report and review of the literature. J Bone Joint Surg Br. May 1999;81(3):462-3. [Medline][Full Text].

  18. Blackwell TL, Krause JS, Winkler T, et al. Spinal Cord Injury Desk Reference: Guidelines for Life Care Planning and Case Management. New York, NY: Demos Medical Pub; 2001.

  19. Brugieres P, Malapert D, Adle-Biassette H, et al. Idiopathic spinal cord herniation: value of MR phase-contrast imaging. AJNR Am J Neuroradiol. May 1999;20(5):935-9. [Medline][Full Text].

  20. Cervical Spine Research Society, Editorial Committee. The Cervical Spine. 2nd ed. Philadelphia, Pa: Lippincott; 1989.

  21. Ellger T, Schul C, Heindel W, et al. Idiopathic spinal cord herniation causing progressive Brown-Séquard syndrome. Clin Neurol Neurosurg. Jun 2006;108(4):388-91. [Medline].

  22. Francis D, Batchelor P, Gates P. Posttraumatic spinal cord herniation. J Clin Neurosci. Jun 2006;13(5):582-6. [Medline].

  23. Gorman PH, Wuolle KS, Peckham PH, et al. Patient selection for an upper extremity neuroprosthesis in tetraplegic individuals. Spinal Cord. Sep 1997;35(9):569-73. [Medline].

  24. Hwang W, Ralph J, Marco E, et al. Incomplete Brown-Séquard syndrome after methamphetamine injection into the neck. Neurology. Jun 24 2003;60(12):2015-6. [Medline].

  25. Longo MJ, Jaffe CC. Images in clinical medicine. Electrical alternans. N Engl J Med. Dec 30 1999;341(27):2060. [Medline].

  26. Hochschuler SH, Cotler HB, Guyer RD, eds. Rehabilitation of the Spine: Science and Practice. St Louis, Mo: Mosby; 1993.

  27. Stover SL. Clinical Outcomes from the Model Systems. Gaithersburg, Md: Aspen Pubs; 1995.

  28. Tattersall R, Turner B. Brown-Séquard and his syndrome. Lancet. Jul 1 2000;356(9223):61-3. [Medline].

Further Reading

Keywords

Brown-Séquard syndrome, Brown-Séquard's syndrome, Brown-Séquard-plus syndrome, hemisection of the spinal cord, hemisection syndrome, partial spinal sensory syndrome

Contributor Information and Disclosures

Author

Carol Vandenakker-Albanese, MD, Director, Post-Polio Clinic, Department of Physical Medicine and Rehabilitation, University of California at Davis Health System; Physical Medicine and Rehabilitation Residency Director, University of California at Davis
Carol Vandenakker-Albanese, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Sports Medicine, American Medical Association, American Paraplegia Society, American Spinal Injury Association, Association of Academic Physiatrists, Florida Society of Physical Medicine and Rehabilitation, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
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, and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

Medical Editor

Elizabeth A Moberg-Wolff, MD, Associate Professor and Pediatric PM&R Fellowship Director, Department of Physical Medicine and Rehabilitation, Medical College of Wisconsin; Program Director, Tone Management and Mobility, Department of Physical Medicine and Rehabilitation, Children's Hospital 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

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Michael T Andary, MD, MS, Residency Program Director, Professor, 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

CME Editor

Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St. Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consort
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

 
 
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