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Solving the puzzle of Brown-Séquard syndrome

Franges, Ellie Z. DNP, RN, ANP-BC, CNRN

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doi: 10.1097/01.CCN.0000694084.86350.93
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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 (S4 and S5).1 An incomplete SCI is the partial preservation of sensory (including position sense, or proprioception), motor, or a combination of sensory-motor function including the lowest sacral segments. A patient with an incomplete SCI will retain some neurologic function (in some cases, only proprioception) below the level of injury. Knowledge of the assessment parameters and patient-care needs is key for assessing and managing incomplete SCIs. This article examines one of the several syndromes related to incomplete 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 is also known as lateral cord syndrome. The most common cause of Brown-Séquard syndrome is trauma, typically penetrating trauma such as a gunshot or stab wound. Other traumatic causes include a unilateral facet fracture and dislocation of the vertebrae, and nontraumatic causes include a tumor, acute disk herniation, and ossification of the posterior longitudinal ligament of the vertebral column. Less common causes include epidural hematomas, multiple sclerosis, radiation, vertebral artery dissection, and I.V. drug use contributing to an epidural abscess.2

The injury causes a transverse hemisection of the spinal cord (half of the cord is transected), with damage to both the ascending and descending tracts on only one side of the cord.1 (See Brown-Séquard syndrome cord damage and associated motor and sensory loss.) 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 that often occurs two to three segments below the injury (lateral spinothalamic tracts). The patient will have varying degrees of ipsilateral loss of tactile discrimination, perception of vibration, and proprioception below the level of injury (posterior columns, including the fasciculus gracilis and fasciculus cuneatus).2

Brown-Séquard syndrome cord damage and associated motor and sensory loss

Although there are no specific data on the incidence of Brown-Séquard syndrome, about 12,000 traumatic SCIs occur in the US each year, and Brown-Séquard syndrome is believed to result from 2% to 4% of these.2,3

Recognizing the syndrome

If Brown-Séquard syndrome is suspected, a thorough primary and secondary survey should be performed according to Advanced Trauma Life Support guidelines.4 The patient's airway, breathing, and circulation must be assessed and supported to prevent secondary injury. The patient's head and neck need to be immobilized and stabilized to prevent further injury. A rapid but careful patient history should be obtained, observing 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.

A complete baseline neurologic assessment should be performed to approximate the level of injury and preserved neurologic function. The patient's muscle function and sensation should be graded using the American Spinal Injury Association (ASIA) Impairment Scale.5 This assessment tool provides a standard neurologic classification of SCI.

Because of the segmental nature of the spinal cord, sensation should be assessed according to dermatomes, which reflect areas innervated by the sensory nerve roots. A careful sensory exam including dermatomes C2 through S4-5 should be performed. A patient with a right-sided cord transection may experience loss of tactile discrimination, perception of vibration, and proprioception (posterior column) on the right side of his or her body below the level of injury. This patient may also have loss of pain and temperature perception on the left side of his or her body 2 to 3 segments below the level of injury.2

The ASIA Impairment Scale incorporates grading of muscle strength from 0 (total paralysis) to 5 (active movement against full resistance). Patients with a right-sided cord transection will have paralysis of all voluntary muscles below the level of injury on the right side of the body. From a motor perspective, Brown-Séquard syndrome can be mistaken for a stroke syndrome.

Critical care nurses can use the following phrase as a memory device, “The limb that moves the least feels the most,” and vice versa.

Because Brown-Séquard syndrome is an incomplete SCI, the patient may not have signs of spinal shock; as a result, early hyperreflexia may develop rather than flaccid paralysis. (See Demystifying spinal shock.)

Patients rarely have signs and symptoms of a pure hemisection. Instead, a patient may exhibit some but not all the typical signs and symptoms or may also exhibit additional signs and symptoms; these cases are referred to as Brown-Séquard-plus syndrome.2

Diagnostic studies

Because Brown-Séquard syndrome is a clinical diagnosis, diagnostic imaging may help pinpoint the etiology. MRI is by far the most useful study because it can help identify actual structural damage and can be useful in evaluating nontraumatic causes.2 An MRI also can help identify ligament injury that may make the spine unstable. An MRI will also show scattered petechial hemorrhages in the white matter.

In patients with contraindications to an MRI, the diagnostic study of choice is a myelogram immediately followed by computed tomography of the spine, which can reveal 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.2 A lumbar puncture with cerebrospinal fluid analysis may be considered if the differential diagnosis suggests multiple sclerosis, transverse myelitis, or tuberculosis.

Initial treatment

Steroids such as methylprednisolone are not recommended in the treatment of SCI.6 However, some healthcare providers may prescribe them on a case-by-case basis rather than following a standard protocol. In a review of the efficacy and safety of steroids in SCI there was no statistically significant improvement with the use of methylprednisolone.7 Of note, because high-dose steroids may increase the risk of pulmonary complications such as pneumonia and pulmonary embolism, as well as the risk of hyperglycemia and infection, these patients should be monitored closely.

Patients with Brown-Séquard syndrome as 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, the healthcare provider must be notified; the patient may need more urgent surgical intervention.

To reduce the risk of secondary injury, continuously assess the patient's vital signs, and aim to keep his or her systolic BP above 90 mm Hg and SpO2 above 94%.8 A goal mean arterial pressure of 85 to 90 mm Hg is recommended for the first week after an SCI.8 If the patient's SCI is mid- to high-cervical—posing a risk to respiratory function—his or her cough reflex and vital capacity (the maximal amount of air that can be exhaled from the point of maximal inspiration) should be evaluated. The level of a patient's injury will determine whether he or she needs ventilator support; patients with an SCI above C4 likely will be ventilator-dependent.1

A manually assisted cough maneuver can help manage secretions in a patient who is not intubated and has a poor cough. Hands should be placed below the patient's rib cage and above the umbilicus and depressed firmly when he or she coughs.1 Brown-Séquard syndrome is an incomplete injury, so most patients need only short-term ventilatory assistance.1

Because patients with SCI often cannot regulate their body temperatures, a temperature-regulating blanket can be provided as needed. To reduce the risks associated with immobility, venous thromboembolism prophylaxis should be administered as prescribed. Patients with SCI have the highest incidence of venous thromboembolism among patients with severe trauma, so guidelines from the Neurocritical Care Society and the Consortium for Spinal Cord Medicine recommend routine thromboprophylaxis as soon as possible.9,10 As prescribed, low-molecular-weight heparin (LMWH) should be administered after primary hemostasis is evident. Alternatives include low-dose or adjusted-dose unfractionated heparin or the combined use of mechanical VTE prophylaxis (such as intermittent pneumatic compression devices) and low-dose unfractionated heparin, adjusted-dose unfractionated heparin, or LMWH.9-11 If the patient has a contraindication to anticoagulants, mechanical VTE prophylaxis should be used, or an inferior vena cava filter may be considered.

Meticulous skin care is essential to reduce the risk of pressure injuries. It is important to remember that in Brown-Séquard syndrome the limb that is strongest feels the least, and therefore is most prone to skin breakdown. Frequent, regular skin assessments must be performed, the patient must be turned and repositioned at least every 2 hours, and pressure-relieving surfaces must be used.12 The skin should be kept clean and dry, and dry skin treated with moisturizers. Nutrition and hydration should be optimized because impaired nutrition and dehydration contribute to pressure injury development.

The patient's pain should be assessed using a valid and reliable pain intensity rating scale and analgesia (typically an opioid such as morphine or fentanyl for acute pain) administered as prescribed. If the patient reports dysesthesias such as a burning sensation, typical of neuropathic pain, gabapentin or pregabalin, a serotonin-norepinephrine reuptake inhibitor, or a tricyclic antidepressant should be administered as prescribed.13

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. Nutrition should be started as soon as possible; if enteral nutrition is needed, short-term tube feeding may be considered, as many patients with Brown-Séquard syndrome regain the ability to eat a normal diet, depending on the level of SCI injury and other factors.

A bowel program should be initiated as prescribed to prevent constipation from immobility, as well as opioid-induced constipation. Adequate fluid intake should be included as part of a bowel maintenance program.

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

Moving on

After initial care, a critical care nurse's focus should shift to preparing the patient for rehabilitation. Physical and occupational therapy should begin early.2 The patient should be mobilized and must participate in activities of daily living as soon as he or she is hemodynamically stable. Getting out of bed helps the patient tolerate an upright position. It is important to help the patient ambulate, as indicated by his or her overall neurologic deficits. Overall recovery varies greatly depending on the cause of injury and the extent of actual cord damage, but there is no single predictor of outcome. Many patients with Brown-Séquard syndrome will have significant functional recovery.14 Optimal nursing care ensures patients 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. Occurring in injuries to the cervical and upper thoracic spinal cord, it is 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. However, in patients with Brown-Séquard syndrome, as a form of incomplete SCI, signs of spinal shock may not be present.




      American Spinal Injury Association (ASIA) motor and sensory scales; Brown-Séquard syndrome; hemisection; incomplete spinal cord injury; paralysis; spinal shock trauma

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