Traumatic Brown-Séquard syndrome: modern reminder of a neurological injury

Abstract

Brown-Séquard syndrome (BSS) presents as an ipsilateral loss of motor function, proprioception and vibratory sensation accompanied by contralateral pain and temperature loss two to three levels below the level of the injury. It is one of the syndromes associated with incomplete transection of the spinal cord. Classic BSS is rare as most patients present with mixed neurological deficits related to damage of the spinal cord and surrounding structures. BSS remains prevalent in areas with high trauma burden, where assaults with sharp weapons are common. We present the case of a man aged 38 years who sustained a stab injury to the left back. BSS was diagnosed. He underwent removal of the weapon in the operating room and had an uneventful recovery to near baseline functional level after a course of rehabilitation. Despite being a rare aetiology, BSS continues to be an excellent reminder to trauma providers of the anatomy and physiology of neuroanatomical tracts.

Background

Brown-Séquard syndrome (BSS) presents as an ipsilateral loss of motor function, proprioception, vibration and light touch sensation, due to the disruption of the descending corticospinal tracts and posterior columns. It is classically accompanied by contralateral loss of pain and temperature sensation from discontinuity of the lateral spinothalamic tracts that decussate two to three levels below the injury, and can also present with a contralateral deficit to crude touch (deep sensation) due to disruption of the anterior spinothalamic tract (figure 1).

Figure 1.

Scheme picturing the three neuroanatomical tracts classically disrupted in Brown-Séquard syndrome. In yellow, the ipsilateral corticospinal tract (descending), which conducts motor function and exits through the anterior columns of the cord. In purple, the ipsilateral dorsal column (ascending), which conduct proprioception and vibratory sensation ipsilaterally until their decussation at the level of the medulla oblongata. And in blue, the contralateral spinothalamic tract (ascending), which conducts sensation to pain and light touch and decussates two levels above their entrance to the cord. This image is original and was created by the artist Ivan Palacios Rey on behalf of the authors of this manuscript.

BSS is most commonly caused by trauma, but other aetiologies such as compressive haematomas, tumours, infiltrative diseases, tuberculosis and multiple sclerosis have also been implicated.^{1 2}

BSS was initially described by Charles-Edouard Brown-Séquard in the late 19th century through a series of laboratory experiments.³ Brown-Séquard attended medical school in Paris, where he obtained his degree in 1846. In this doctoral thesis, he hypothesised that sensory pathways in the spinal cord crossed over to the opposite side to ascend to the encephalon, an idea that was considered radical at the time. Through a series of ablation experiments and anatomic sections on animals, he established that the ventral root conducted motor function whereas the dorsal roots conducted the sensorium. However, it was not until late 1850s when after refining his observations, he was able to define the triad as we know it today.

BSS is considered one of the classic syndromes of incomplete spinal cord injury. However, only about 3% of patients present with classic syndrome. This has prompted clinicians to use the term ‘Brown-Séquard-plus’ when other atypical neurological findings are present on the neurological exam.⁴

We describe the case of a patient who presented to a level 1 trauma centre with BSS secondary to a stab wound to the left back.

Case presentation

A man aged 38 years with no significant medical history presented to our level 1 trauma centre after being assaulted during an armed robbery. He sustained a single stab wound with a 20 cm kitchen knife to the left midthoracic back. He was transported to our centre in a right lateral decubitus position, with the knife in place. On arrival, he was awake and alert but complained of severe pain to the site of injury.

He had accompanying paraesthesias in the right lower extremity and hemiparesis of the left lower extremity. The primary survey revealed a patent airway with bilaterally equal breath sounds. The patient remained haemodynamically stable, with palpable symmetric pulses in all four extremities, and no other circulatory derangements or obvious sites of bleeding. On the deficit assessment, he was awake and oriented to person, place and time. He had symmetric and bilaterally pupils reactive to light and accommodation and a Glasgow Coma Scale score of 15. However, he was unable to move the left lower extremity and had decreased sensation in both lower extremities. On exposure of the back a 20 cm kitchen knife was in place, penetrating approximately 7 cm at the level of the mid-left thoracic back (figure 2). No other injuries were encountered. Adjunct studies including a posteroanterior chest X-ray and an extended focused assessment with sonography in trauma showed no other injuries. Two grams of cefazolin and tetanus toxoid were given, and a CT scan of the chest and abdomen were done with the penetrating weapon in situ. He was kept in prone position to avoid worsening of the injury. During the secondary survey he had weakness in his left lower extremity (motor function 0/5) with associated decreased sensitivity to light touch, temperature and vibration. He also had decreased sensitivity to touch and temperature on his right lower extremity with normal motor function (5/5) below the distribution of the T11 dermatome. Deep tendon reflex examination was normal on both upper extremities (biceps, brachioradialis) and the right lower extremity (2+) but deep tendon reflexes were decreased (1+) on the left lower extremity (patellar, Achilles).

Figure 2.

(A),(B),(C). Clinical pictures showing patient lying in the prone position with the knife in place.

Investigations

Initial blood work showed mild leukocytosis (12.55×109 cells/mL). The rest of the laboratory workup was within normal limits. CT scan revealed a knife penetrating a total depth of 72 mm at the level of T11 with a 17-degree downward trajectory from the horizontal plane. The knife traversed the paraspinal muscles, entered the spinal canal between T10 and T11 and was lodged at the vertebral body of T11 (figures 3 and 4). There were no intra-abdominal or intrathoracic injuries noted.

Figure 3.

(A),(B),(C). CT scan showing serial axial images in prone position at the level of the injury, following the trajectory of the weapon. Note how the tip of the knife is lodged at the level of the T11 vertebral body.

Figure 4.

(A) CT scan scout film showing the knife in place with its angulation. (B) Sagittal images showing spinal cord transected by knife in situ.

He was taken to the operating room for removal of the weapon and washout of the wound. After successful removal, haemostasis was achieved with monopolar electrocautery and the skin was loosely approximated to allow fluid collections to drain out. He was transferred to the surgical intensive care unit for further neurological monitoring. After removal of the knife, he continued to complain of left lower extremity weakness and right lower extremity paresthesias.

A thoracolumbar spine MRI, done postoperatively, showed a clear hemi-injury to the left side of the spinal cord at the level of T11 with no significant intraspinal haematoma or cord compression. He had an associated fracture of the left T10 lamina and T10-T11 facets (figures 5 and 6).

Figure 5.

MRI images showing sagittal views in T2 (A and B) and T1 (C and D) sequences of the spine and spinal cord at the level of injury (yellow circle).

Figure 6.

MRI images showing axial cuts in T1 (A) and T2 (B) sequence. Demonstrating the spinal injury with the trajectory marked by yellow arrow.

During the tertiary survey, neurological examination showed an intact mental status and cognition, pupils were symmetric and equally reactive to light and accommodation, cranial nerve examination was unremarkable and cerebellar function was intact. His motor function and sensory examination were remarkable for significant weakness of the left lower extremity (motor function 1/5), affecting the hip and knee extensors and flexors, as well as ankle dorsal and plantar flexion. Also, decreased sensation to vibration, proprioception and touch on the ipsilateral side were noted. On the right lower extremity, there was a notable decrease in sensation to pinprick, temperature and deep touch, but vibratory sensation was unremarkable. Abnormal sensation was consistent with the distribution of the T11-T12 dermatomes and affected up to about 10 cm below the level of the umbilicus on the anterior abdominal wall and to the level of the lumbar region on the back. Sensation and motor function above these levels were unremarkable. He was unable to void but had preserved rectal continence and sphincter function.

Differential diagnosis

The diagnosis of BSS was confirmed. Other diagnoses considered at this time were posterior cord injury, central cord syndrome and an incomplete spinal injury (table 1).

Table 1.

Comparison between clinical characteristics of different spinal cord syndromes

Type	Syndrome	Classic aetiology	Prognosis
Anterior cord	Bilateral paraplegia Pain and temperature loss Proprioception and vibration intact ±Bladder dysfunction	Spinal infarction, disc herniation, radiation myelopathy.	Poor
Central cord	Bilateral motor weakness Predominantly in upper extremities ±Sensory dysfunction ±Bladder dysfunction	Syringomyelia, spinal tumours, cervical spondylosis myelopathy, trauma, neck hyperextension.	Variable
Posterior cord	-Bilateral vibration and proprioception deficit ±Bladder dysfunction -Intact motor function	Tabes dorsalis, Frederich’s ataxia, subacute combined degeneration, AIDS, epidural metastases, spondylotic myelopathy, multiple sclerosis.	Variable
Complete transection	Complete loss of sensation below the level of injury Complete paralysis below the level of injury	Trauma, infarction, transverse myelitis, abscess, tumour.	Poor
Brown Séquard syndrome	Ipsilateral motor deficit, vibration and proprioception Contralateral pain and temperature 2–3 levels below injury	Trauma, tumours, causing spinal cord hemisection or compression.	Good
Cauda equina syndrome	Saddle anaesthesia Asymmetric radicular pain Reduced DTRs Bladder and rectal dysfunction	Disc herniation, arachnoiditis, tumours, spinal stenosis, trauma.	Reserved Requires surgical intervention

Adapted from the Textbook of the Cervical Spine.¹⁵

DTR, Deep tendon Reflexes.

Post-treatment course

The patient was assessed by a spine surgeon, who determined that no further surgical intervention was required. He remained stable, continued to recover and was started on physical therapy and rehabilitation. Given his inability to void, intermittent urinary catheterisations were required during the first days; however, he was eventually able to void spontaneously and was discharged to an acute rehabilitation unit requiring the assistance of a wheelchair.

Outcome and follow-up

He remained in the inpatient acute rehabilitation unit for 17 days. During his stay, his left lower extremity strength improved considerably on hip extension and flexion and his urinary retention resolved. He was seen in clinic 3 months after the injury, and at that point he demonstrated considerable recovery in the motor function of the left lower extremity to 4/5, was able to ambulate with crutches and reported improvement in the sensation as well.

Discussion

The incidence of spinal cord injury in the USA is close to 40 per million people a year, almost double of what is reported worldwide.⁵ It occurs more frequently in young males, although cases have also been reported in the paediatric and elderly populations.^{6 7} Despite this, the pure form of BSS is rarely seen. This stems from the fact that most spinal cord lesions are caused by blunt trauma, motor vehicle collisions, falls and gunshot injuries, which by the nature of their mechanism usually produce more extensive damage to the surrounding structures with mixed clinical presentations. Thus, clinicians practising in areas with high trauma burden should have a high index of suspicion for this rare injury, especially in areas where sharps may be frequently used as assault weapons.⁸

Despite its seemingly ominous clinical presentation, BSS is known to carry a good prognosis for recovery after an appropriate course of rehabilitation, like we saw in our patient.⁹ Therapy is mostly focused on supportive care in the acute setting. Data regarding the efficiency of steroids are still controversial, although the American Association of Neurological Surgeons does not recommend its use.¹⁰ In our institutional experience, the use of steroids has been abandoned and is limited to selected patients with other concomitant indications. The benefit on the use of antibiotics has also been controversial and practices vary between institutions.

Surgical management varies on individual presentation but is generally reserved to those cases that require the removal of foreign objects, and those that develop cerebrospinal fluid fistula, or expanding lesions that require decompression.¹¹

As the mechanism of trauma that causes spinal cord injury leans towards more high energy impact scenarios, the existence of BSS has passed to become almost a myth, encountered only in neuroanatomical textbooks. However, this case serves as a reminder that we need to maintain a high level of suspicion when taking care of patients with penetrating injuries to the back.

In our case, the specific clinical presentation as well as the physical findings deviate slightly from a classic BSS. Our patient presented bilateral deficit of touch, which is explained by the disruption of posterior column on the left, as well as disruption of the anterior spinothalamic tract on the left, which manifested as the right-sided deficit. We believe that the angulation of the knife might have caused involvement of the surrounding neural tracts, altering the level of the sensory abnormalities that were encountered. This case once again highlights that classic BSS is rarely encountered in its purest form.

Understanding the pathophysiology and anatomical landmarks that led to this particular syndrome will allow us to provide the appropriate interventions in a timely manner. To date, there is no evidence of pharmacological interventions that improve the regenerative capacity of the central nervous system, although many are being studied.^12–14 Therefore, the role of the surgeon is limited to providing haemodynamic support with the goal of maintaining an optimal perfusion to the spinal cord to reduce the production of oxidative metabolites that may cause further damage.

Learning points.

• Brown-Séquard syndrome (BSS) presents as an ipsilateral loss of motor function, proprioception and vibratory sensation accompanied by contralateral pain and temperature loss two-three levels below the level of injury.

• Most common cause of BSS is trauma.

• The most common presentation of BSS is that of a mixed neurological syndrome with nearly all described components of BSS plus additional deficits referred to as BSS-plus.

• Despite a seemingly ominous clinical presentation, BSS has a good prognosis when the appropriate course of rehabilitation therapy is initiated in a timely manner.