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Brown-Sequard Syndrome
Overview

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.(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

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.
Next: Anatomy

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.
Previous
Next: Anatomy

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.
[7]
Previous
Next: Anatomy

Etiology

T ti
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.

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]

Cervical spondylosis

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

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]
Previous
Next: Anatomy

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.
[18] 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.
[19]
Previous
Next: Anatomy

Prognosis
Prognosis for significant motor recovery in Brown-Séquard syndrome is good.
[19] 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

[20] :

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.
[21] ) 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.
[22]

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
postoperative infection.
Previous
Clinical Presentation

 
 

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

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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, Association of Academic Physiatrists, North American Spine
Society

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
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