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What is Brown-Séquard syndrome?

Franges, Ellie RN, APRN-BC, CNRN, MSN

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doi: 10.1097/01.CCN.0000351581.51493.c9
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In Brief

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Spinal cord injury (SCI) is a significant challenge for healthcare providers. A complete SCI is defined as the loss of all sensory and voluntary motor function below the level of the injury or lesion, including the lowest sacral segments (S-4 and S-5).1 An incomplete SCI occurs when there's partial preservation of sensory (including position sense), motor, or a combination of sensory-motor function including the lowest sacral segments. Therefore, a patient with an incomplete SCI will retain some neurologic function (in some cases, only position sense) below the level of injury. Incomplete injuries are often more difficult to assess and manage, so knowing the assessment parameters and patient care needs is key. In this article, I'll examine one of the several syndromes related to SCI, Brown-Séquard syndrome.

First described in the 1840s by Dr. Charles-Edouard Brown-Séquard, this syndrome results from an injury to half of the spinal cord, and also is known as lateral cord syndrome. The most common cause of Brown-Séquard syndrome is trauma, typically penetrating trauma such as a gunshot wound or stabbing. Other traumatic causes include a unilateral facet fracture dislocation of the vertebrae, and nontraumatic causes such as tumor, acute disc herniation, and ossification of the posterior longitudinal ligament of the vertebral column. Less common causes, reported in case studies, include epidural hematomas, multiple sclerosis, radiation, vertebral artery dissection, and I.V. drug use (which can contribute to epidural abscess).2

The injury causes a transverse hemisection of the spinal cord (half of the cord is transected from north to south), with damage to both the ascending and descending tracts on only one side of the cord.1 (See What happens in Brown-Séquard syndrome?) The injury results in ipsilateral (on the same side as the cord damage) loss of voluntary motor function below the level of injury (lateral corticospinal tract) with contralateral (opposite side of the cord damage) loss of pain and temperature sensation below the injury (lateral spinothalamic tracts). The patient will have varying degrees of loss of perception of touch, vibration, and position below the level of injury (posterior columns, which include the fasciculus gracilis and fasciculus cuneatus).

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Figure:
What happens in Brown-Séquard syndrome?Source: Hickey J. The Clinical Practice of Neurological and Neurosurgical Nursing. 6th ed. Lippincott Williams and Wilkins; 2008.

Although there's no specific data on the incidence of Brown-Séquard syndrome, about 11,000 traumatic SCIs occur in the United States each year, and Brown-Séquard syndrome is believed to account for 2% to 4% of these.2

Recognizing the syndrome

If you suspect that your patient has Brown-Séquard syndrome, perform a thorough primary and secondary survey according to advanced trauma life support guidelines. Assess and support the patient's airway, breathing, and circulation to prevent secondary injury. Immobilize and stabilize the patient's head and neck to prevent further injury. Obtain a rapid but careful patient history, paying attention for clues that might provide important information to aid the diagnosis. The treatment goals in acute care are to preserve or improve function, prevent secondary injury, and minimize complications.

Perform a complete baseline neurologic assessment to approximate the level of injury and preserved neurologic function. Rate the patient's function and impairment by using the American Spinal Injury Association (ASIA) motor and sensory scales. This assessment tool provides a standard neurologic classification of SCI. Because of the segmental nature of the spinal cord, the level of sensation assessed according to dermatomes, which reflect areas innervated by the sensory nerve roots.

If your patient has a right-sided cord transection for example, he'll have paralysis of all voluntary muscles below the level of injury on the right side of the body. (From a motor perspective, Brown-Séquard can be mistaken for a stroke syndrome.) The ASIA motor and sensory scale incorporates a scale for grading muscle strength from 0 (total paralysis) to 5 (active movement against full resistance). Because this is an incomplete SCI, the patient may not have signs of spinal shock; as a result, you'll see early hyperreflexia rather than flaccid paralysis. (For more information, see Demystifying spinal shock.)

Perform a careful sensory exam including dermatomes C2 through S4-5. Going back to your patient with a right-sided cord transection, you find he's lost perception of touch, vibration, and position on the right side of his body below the level of injury; he's also lost pain and temperature perception of the left side of his body below the level of injury. You can remember these findings as “the limb that moves the least feels the most,” and vice versa.

Patients rarely have signs and symptoms of a pure hemisection; you may also note signs and symptoms consistent with a posterior column injury.

Diagnostic studies

Because Brown-Séquard syndrome is a clinical diagnosis, diagnostic imaging may help pinpoint the etiology. Magnetic resonance imaging (MRI) is by far the most useful study because its sensitivity can help identify actual structural damage and can be useful in nontraumatic causes. An MRI also can help identify ligament injury that may make the spine unstable. The MRI also will show scattered petechial hemorrhages in the white matter.

In patients with contraindications to an MRI, such as an implanted cardiac pacemaker or implantable cardioverter defibrillator, the diagnostic study of choice is a myelogram immediately followed by computed tomography of the spine, which reveals nerve tissue destruction on one side of the spinal cord.

No lab studies are specific to Brown-Séquard syndrome, but if the cause of the SCI is unclear, the patient might be tested for infection or neoplasm. A lumbar puncture with cerebrospinal fluid analysis may be considered if the differential diagnosis suggests multiple sclerosis, transverse myelitis, or tuberculosis.

Initial treatment

The use of high-dose steroids is controversial, so the healthcare provider may prescribe them on a case-by-case basis rather than following a standard protocol. In incomplete SCIs, high-dose methylprednisolone may improve outcomes.1 However, high doses of steroids raise the patient's risk for infection, so this therapy typically isn't used in patients who've suffered a penetrating injury. If the patient's SCI is the result of a nonpenetrating, noninfectious clinical syndrome, he may be given high-dose steroids in an attempt to improve function.

If steroids are prescribed, start the infusion as soon as possible, and no later than 8 hours after the injury.3 Because high-dose steroids may increase the risk of pulmonary complications such as pneumonia and pulmonary embolism, monitor your patient closely.

Patients whose Brown-Séquard syndrome is the result of a penetrating injury also need to be treated for bleeding and direct tissue damage. Early surgical management may be needed to obtain hemostasis and close the wound, and to stabilize the spine if indicated based on diagnostic imaging studies. If the patient's neurologic status deteriorates, notify the healthcare provider; the patient may need more urgent surgical intervention.

To reduce the risk of secondary injury, continuously assess your patient's vital signs, and aim to keep his systolic BP above 90 mm Hg and SpO2 above 94%. If his SCI is mid- to high-cervical—posing a risk to respiratory function—evaluate his cough reflex and vital capacity (the maximal amount of air that can be exhaled from the point of maximal inspiration). The level of his injury will determine whether he'll need ventilator support; patients with an SCI above C4 likely will be ventilator-dependent.

Use a manually assisted cough maneuver to help manage secretions in a patient who's not intubated and has a poor cough. Place your hands below the patient's rib cage and above the umbilicus, and depress firmly when he coughs. Brown-Séquard syndrome is an incomplete injury, so most patients need only short-term ventilatory assistance.

Because patients with SCI often can't regulate their body temperatures, provide a temperature-regulating blanket as needed. To reduce the risks of immobility, provide venous thromboembolism prophylaxis as prescribed. Patients with SCI who don't receive thromboprophylaxis have the highest incidence of deep vein thrombosis among all hospitalized patients, so the American College of Chest Physicians recommends routine thrombophylaxis for these patients.4 As prescribed, administer low-molecular-weight heparin (LMWH) after primary hemostasis is evident. Alternatives include the combined use of intermittent pneumatic compression and either low-dose unfractionated heparin or LMWH.4 If the patient has a contraindication to anticoagulants, a vena cava filter may be considered.

Provide meticulous skin care to reduce the risk of pressure ulcers. Remember in Brown-Séquard syndrome, the limb that's strongest feels the least, so the side with the most strength (and the lack of sensation) is most prone to skin breakdown. Perform frequent, regular skin assessments, turn and reposition the patient at least every 2 hours, and use pressure-relieving surfaces to reduce or relieve pressure on skin and subcutaneous tissues.5 Make sure the skin is kept clean and dry and treat dry skin with moisturizers. Optimize nutrition and hydration because impaired nutrition and dehydration contribute to pressure ulcer development.

Assess the patient's pain using a valid and reliable pain intensity rating scale, and administer analgesia (typically morphine or fentanyl for acute pain) as prescribed. If the patient reports burning type dysesthesias, typical of neuropathic pain, administer gabapentin, an antiepileptic drug, or a tricyclic antidepressant as prescribed.6

The patient should have a gastric tube to reduce the risk of abdominal distension secondary to paralytic ileus, a common complication after SCI. A distended abdomen interferes with adequate respirations. Begin nutrition as soon as possible; if enteral nutrition is needed, consider short-term tube feeding, as most patients with Brown-Séquard syndrome will be able to eat a normal diet.

Initiate a bowel program with regular stool softeners and a daily suppository to prevent constipation from immobility, as well as opioid-induced constipation. Ensure adequate fluid intake as part of a bowel maintenance program.

The patient will have an indwelling urinary catheter, which can be removed after the acute injury phase. Assess the patient's ability to void, and determine if a long-term bladder management program is needed.

Moving on

After initial care, your focus is to prepare the patient for rehabilitation. Begin physical and occupational therapy early and encourage the patient to mobilize and participate in activities of daily living as soon as he's hemodynamically stable. Getting out of bed helps the patient tolerate an upright position. Help him ambulate as indicated by his overall neurologic deficits. Overall recovery varies greatly and there's no one predictor of outcome. However, with optimal nursing care, your patient will have the best chance at a good outcome.

Demystifying spinal shock

Spinal shock is a clinical syndrome often seen in major SCI, and usually is the result of a rapid progressive lesion. Affecting the cervical and upper thoracic spinal cord, it's caused by a temporary interruption of the sympathetic function, leaving parasympathetic function unopposed. Characteristic findings are flaccid paralysis, loss of cutaneous and deep tendon reflexes, and anesthesia below the level of injury.1

Patients who initially have a flaccid paralysis develop spasticity below the level of injury, consistent with an upper motor neuron injury. Spinal shock can last for days to months; the return of reflexive activity below the level of the lesion signals the end of spinal shock.

REFERENCES

1. Hickey J. The Clinical Practice of Neurological and Neurosurgical Nursing. 6th ed. Lippincott Williams and Wilkins; 2009.
2. Vandenakker-Albanese C, Zhao H. Brown-Séquard syndrome.http://emedicine.medscape.com/article/321652-overview.
3. Beeson M. Brown-Séquard syndrome.http://emedicine.medscape.com/article/791539-overview.
4. Geerts WH, Bergqvist D, Pineo GF, et al. Prevention of venous thromboembolism: American College of Chest Physicians evidence-based clinical practice guidelines (8th ed). Chest. 2008;133(suppl 6):381S–453S.
5. Institute for Healthcare Improvement. Prevent pressure ulcers.http://www.ihi.org/IHI/Programs/Campaign/PressureUlcers.htm.
6. Barker E. Neuroscience Nursing: A Spectrum of Care. 3rd ed. Mosby Elsevier; 2008.

RESOURCES

Blumenfeld H. Neuroanatomy Through Clinical Cases. Sunderland, Mass; Sinauer and Associates; 2002.
    Lindsay KW, Bone I. Neurology and Neurosurgery Illustrated. 4th ed. Philadelphia, PA: Churchill Livingstone; 2004.
      © 2009 Lippincott Williams & Wilkins, Inc.