Traumatic atypical Brown-Sequard syndrome: case report and literature review

Traumatic atypical Brown-Sequard syndrome: case report and literature review

Clinical Neurology and Neurosurgery 105 (2003) 143 /145 www.elsevier.com/locate/clineuro Case report Traumatic atypical Brown-Sequard syndrome: cas...

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Clinical Neurology and Neurosurgery 105 (2003) 143 /145 www.elsevier.com/locate/clineuro

Case report

Traumatic atypical Brown-Sequard syndrome: case report and literature review Erle Lim a,*, Y.S. Wong b, Y.L. Lo c, S.H. Lim c a

Department of Medicine, Alexandra Hospital, 378 Alexandra Road, Singapore 159964, Singapore b Department of Orthopedic Surgery, Alexandra Hospital, Singapore 159964, Singapore c Department of Neurology, Singapore General Hospital, Singapore Received 19 September 2002; accepted 13 February 2003

Abstract A man was kicked on the neck, 10 days after which he noted right-sided numbness. Clinically, he had diminished deep tendon reflexes over the left upper limb, absent left superficial abdominal reflexes, a left extensor plantar response, mild left hemiparesis, diminished pinprick, temperature and vibratory sensation up to the right T4  5 dermatome and diminished proprioceptive sensation in the right upper and lower limbs. Cervicothoracic magnetic resonance imaging (MRI) revealed a left C6  7 posterolateral disc prolapse with indentation and oedema of the cord at the same level. He was given intravenous dexamethasone, with mild resolution of his motor but not his sensory symptoms. Transcranial magnetic stimulation and evoked potentials performed 3 days later were unremarkable. He was discharged soon after, preferring to seek traditional therapy in his country. We attempt to explain the anatomical basis for his clinical signs, review the literature for similar cases, and examine the usefulness of available treatment and investigations. # 2003 Elsevier Science B.V. All rights reserved. Keywords: Atypical; Brown-Sequard; Trauma

1. Case history A 37-year-old construction worker was admitted to the Orthopedic service with complaints of right sided numbness extending from his foot up to the nipple line. He gave a history of having been assaulted 1 week prior to admission, sustaining a kick to the neck posteriorly. Numbness developed 3 days later. He denied limb weakness, and had no bowel or bladder disturbances. Clinical examination 7 days after the event was significant for areflexia in the left upper limb, an extensor plantar response on the left, absent superficial abdominal reflexes on the left and a mild left hemiparesis. The sensory examination was remarkable for diminution of pinprick and temperature sensation on the right side up to T4 dermatome, reduced vibratory * Corresponding author. Tel.: /65-379-3461; fax: /65-379-3540. E-mail address: [email protected] (E. Lim).

sensation up to the right T5 dermatome, and reduced proprioceptive sensation on the right, lower limbs more affected than the upper. There were no bowel or bladder disturbances. The cranial nerve examination was unremarkable. Magnetic resonance imaging (MRI) of the cervical and thoracic spine showed a small left-sided posterolateral disc prolapse at the level of the sixth and seventh cervical vertebrae, causing thecal and cord indentation. There was a corresponding increased signal at that level on T2-weighted sagittal section, consistent with cord oedema. (Fig. 1). Transcranial magnetic stimulation, nerve conduction, and median and tibial somatosensory evoked potential studies performed 10 days after onset of symptoms were within normal limits. He was commenced on intravenous dexamethasone 4 mg twice a day for a week, after which he was given oral prednisolone 30 mg once a day for a week. This resulted

0303-8467/03/$ - see front matter # 2003 Elsevier Science B.V. All rights reserved. doi:10.1016/S0303-8467(03)00009-X

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2. Discussion

Fig. 1. Sagittal T2-weighted MRI showing disc prolapse at C6  7, with hyperintensity in the cervical cord.

in mild improvement in his motor but not his sensory symptoms. Surgical treatment was not considered as he had only mild neurological deficits and the expected benefits would not have outweighed the risks. It is unfortunate that our patient refused follow-up assessment and repeat imaging, to demonstrate clinical and radiologic resolution.

Post-traumatic Brown-Sequard syndrome has been well described in the literature. The classical syndrome, which is the consequence of hemisection of the spinal cord, consists of ipsilateral weakness and loss of proprioceptive and vibratory sensation on the same side, due to disruption of the corticospinal tracts and dorsal columns, respectively. Loss of pain and temperature sensation occurs on the contralateral side because the involved spinothalamic tract carries these modalities of sensation from the opposite side. This syndrome is named for Charles Edouard Brown-Sequard (1817 / 1894), who delineated the sensory pathways in the spinal cord [1]. More often, the clinical syndrome is incomplete, with ipsilateral weakness and contralateral loss of pinprick and temperature sensation, but intact proprioceptive and vibratory sensation. This results from compression of the spinal cord sparing the dorsal columns [2,3]. Reports of Horner’s syndrome in addition to the above findings [2] are attributed to the involvement of ipsilateral involvement of descending sympathetic fibers within the cervical spinal cord. Our patient had left-sided weakness and right-sided sensory loss to all modalities of sensation. We postulated that the kick to the left posterolateral aspect of his neck probably brought about the left posterolateral disc prolapse at C6  7 level. This might have caused direct damage to the left ventral and lateral corticospinal tracts as well as the spinothalamic tracts. The loss of proprioceptive and vibratory sensation on the contralateral side of injury is atypical. We postulate that there was indirect damage to the right dorsal columns through a contrecoup injury (Fig. 2).

Fig. 2. (a) Left posterolateral disc prolapse. (b) Left posterolateral disc prolapse causing compression of left corticospinal and spinothalamic tracts and right dorsal columns. The circled areas are postulated to be involved in causing the clinical signs.

E. Lim et al. / Clinical Neurology and Neurosurgery 105 (2003) 143 /145

The second point of interest in our patient was that he had sensory loss to T4  5 level despite a neck trauma with spinal cord injury at C6  7. This is most likely due to the somatotopic representation within the spinal cord where the sacral, leg and thoracic areas were more lateral, thus more susceptible to lateral injury (Fig. 2). Other papers describing post-traumatic Brown-Sequard syndrome have also described abnormal evoked potentials [4]. Normal neurophysiologic findings could be due to improvement following administration of glucocorticoid therapy leading to resolution of oedema. It is conceivable that the somatosensory evoked potential study was not sensitive enough to detect mild dorsal column dysfunction. False negative somatosensory evoked potential studies have been reported in the literature [5 /7]. By the same token, transcranial magnetic stimulation is not a foolproof method of diagnosing pyramidal dysfunction [8,9]. Motor evoked potential latencies measure the fastest conducting fibers. Hence, subtle abnormalities may not show up.

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References [1] Aminoff MJ. Brown-Sequard and his syndrome. J Hist Neurosci 1996;5(1):14 /20. [2] Koehler PJ, Endtz LJ. The Brown-Sequard syndrome: true or false. Arch Neurol 1986;43:921 /4. [3] Taylor RG, Gleave JRW. Incomplete spinal cord injuries-with Brown-Sequard phenomena. J Bone Jt Surg Br 1957;39:438 /50. [4] McCarron MO, Flynn PA, Pang KA, Hawkins SA. Traumatic Brown-Sequard-plus syndrome. Arch Neurol 2001;58(9):1470 /2. [5] Ben-David B, Haller G, Taylor P. Anterior spinal fusion complicated by paraplegia: a case report of a false-negative somatosensory evoked potential. Science 1986;12:536 /9. [6] Ginsberg HH, Shetter AG, Raudszess PA. Postoperative paraplegia with preserved intraoperative somatosensory evoked potentials. J Neurosurg 1985;63:296 /300. [7] Lesser RP, Raudzens P, Luders H, et al. Postoperative neurological deficits may occur despite unchanged intraoperative somatosensory evoked potentials. Ann Neurol 1986;19:22 /5. [8] Padberg AM. Spinal cord monitoring: current state of the art. Orthop Clin North Am 1999;30(3):407 /33 (viii). [9] Claus D, Brunholzl C, Kerling FP, Henschel S. Transcranial magnetic stimulation as a diagnostic and prognostic test in amyotrophic lateral sclerosis. J Neurol Sci 1995;129(Suppl.):30 /4.