Case 2: Acute paralysis in a 10-year-old girl

An otherwise healthy 10-year-old girl presented with acute onset of lower extremity paresthesia, weakness and altered bladder function following the performance of long jump at school. Before and at the time of the jump, she did not complain of any pain or trauma, and was able to walk normally. Approximately 1 h after the jump however, she experienced a gradual onset of weakness and decreased sensation in her lower extremities. When she presented to the pediatric emergency department 12 h later, she was unable to walk. She complained of mild lower back pain and saddle paresthesia. Her vital signs were stable; she was afebrile, alert and oriented. Her cranial nerves and upper extremity examination were normal. Her reflexes were absent at the knee and ankle bilaterally. Strength was preserved at her hips (5 of 5), slightly decreased at her knees (3 of 5) and significantly decreased at her ankles (1 to 2 of 5 plantar- and dorsiflexion). Her sensation to light touch and pinprick was decreased in an L3 to S1 distribution bilaterally. She had no rectal tone. She had not voided since before the jump. Further investigation revealed the diagnosis. The clinical findings were consistent with both the conus medullaris (absent ankle reflexes, early sphincter involvement, symmetrical saddle distribution of sensory deficits, mild back pain, normal proximal muscle strength) and cauda equina (absent patellar reflexes, normal proximal muscle strength) syndromes. Emergent magnetic resonance imaging (MRI) of the spinal cord revealed an area of T2 hyperintensity involving the conus medullaris from T12 to L1 (Figure 1) and was consistent with the clinical findings. The lesion occupied the anterior and centre of the cord, sparing the periphery. It showed diffusion restriction with no evidence of enhancement in the postcontrast scan. The anterior spinal artery opposite this level was slightly hyperintense on the T1-weighted sequence. The remainder of the cord and vertebral column were normal. Magnetic resonance imaging of spine, T2 sequence, sagittal view showing hyperintense signal consistent with infarct at T12 to L1 level extending down to the conus medullaris The finding of diffusion restriction in the T12 to L1 region of the spinal cord was consistent with acute infarct and edema. Further investigations including MRI of the head, echocardiogram, thrombophilia screening and cerebrospinal fluid studies were normal. On follow-up MRI/magnetic resonance angiogram, postischemic gliosis was observed in the region of the infarct and no evidence of dural arteriovenous malformation was found. Spinal cord and vertebral column injuries are uncommon in pediatrics; the incidence ranges from 1% to 10% of all spinal injuries reported (1). Spinal cord injury without radiographic abnormality (SCIWORA) is a pediatric syndrome that is observed in one-third of pediatric traumatic spinal cord injuries (1). Initially described in the era before MRI, SCIWORA is diagnosed in children with signs of spinal cord dysfunction as a result of trauma but no evidence of skeletal injury on imaging tests (normal plain radiographs and computed tomography). The causes of neurological compromise observed in SCIWORA include vascular injury (occlusion, spasm, infarction), segmental spinal instability, ligamentous injury, disc impingement or incomplete neuronal destruction (2). Spinal cord infarction in children is rare. Risk factors for this condition were outlined after a recent review of 108 case reports; the most common etiologies were found to be bacterial meningitis, fibrocartilaginous embolism, umbilical arterial catheters and minor trauma (3). There are a small number of case reports describing children with SCIWORA following minor trauma; the exact etiology of spinal cord infarction following minor trauma is not well understood (3). A proposed mechanism is that the relatively inelastic spinal cord is strained inside the more flexible spinal column during either hyperflexion or hyperextension resulting in reactive vasospasm or compression of vertebral and/or spinal arteries. Hyperextension as a proposed mechanism for spinal cord infarction is similar to that associated with ‘surfer's myelopathy’ (SM). SM was first described in a 2004 series of novice surfers who experineced acute onset of symmetrical leg weakness (4). SM is an atraumatic spinal cord injury resulting from prolonged spinal hyperextension while lying prone; spinal cord ischemia results from avulsion of perforating vessels, vasospasm of the artery of Adamkiewicz or transient vascular hypoperfusion in watershed regions due to spinal cord tension (4). Sudden hyperextension of the spine occurs during the first phase of long jump; the MRI findings in our patient were identical to those described for SM. Clinical outcomes of SM range from near complete recovery to persistent paraplegia and neurogenic bladder (4). Our patient was initially treated with high-dose intravenous steroids and low-dose acetylsalicyclic acid. She subsequently received intensive rehabilitation, physiotherapy and bladder catheterization over a 72-day hospital stay. One year postinjury, she walks independently using a left ankle foot orthotic due to persistent foot drop. She has decreased sensation below her knees bilaterally, decreased ankle and knee jerk and neutral plantar reflexes. She performs clean intermittent catheterization for bladder care and her bowel function is normal. She takes baclofen daily. A full neurological examination with findings of weakness, decreased sensation, altered reflexes and decreased rectal tone will identify spinal cord dysfunction at the bedside. Significant spinal cord injury can occur in the absence of bony trauma in pediatric patients. Spinal cord infarction is a rare cause of acute paralysis in children and may occur following minor trauma. Prompt referral to a pediatric tertiary care centre with capacity for MRI, subspecialty care and rehabilitation is necessary for children with spinal cord injury.

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